Transcript Upper Gastrointestinal Tract - Nutrition and Food Technology-just

Upper Gastrointestinal Tract
Chapter 16
© 2007 Thomson - Wadsworth
Upper GI – A&P
• GI tract – long tube ~ 15 ft.
• Upper GI – mouth, pharynx,
esophagus, stomach
• Accessory organs – pancreas,
biliary system, liver
• Four basic functions: motility,
secretion, digestion, absorption
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© 2007 Thomson - Wadsworth
Upper GI – A&P
• Motility - movement of food by
propulsion and contractions
• Secretions – water, electrolytes,
enzymes, bile salts, mucus
• Digestion – complex molecules
converted to simplest form
• Absorption – basic molecules,
electrolytes, water, vitamins & minerals
provide nutrients to the cells
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Upper GI – A&P
• Regulated through
neurotransmitter secretion
e.g. acetylcholine, substance P,
serotonin, dopamine, CCK,
somatostatin etc.
See Table 16.1 for others
• Parasympathetic impulses carried
by vagus nerve
© 2007 Thomson - Wadsworth
© 2007 Thomson - Wadsworth
Upper GI – A&P
• Oral Cavity Motility
Mastication
• Oral Cavity Secretions
Saliva from 3 sets of salivary glands
• Water
• Electrolytes - sodium chloride,
bicarbonate, potassium
• Proteins - enzymes, mucus, lysozymes
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Upper GI – A&P
• Saliva – functions
Moistening/lubrication
Initial digestion of CHO
Antibacterial protection
Enhances taste
Serves as a buffer
Oral hygiene
Assisting speech
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Upper GI – A&P
• Esophagus
Sphincters at either end
Four layers of tissue: mucosa,
submucosa, muscle, adventitia
Chief function is motility
Swallow phases:
• Oral preparatory phase
• Oral
• Pharyngeal
• Esophageal
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Upper GI – A&P
• Esophagus
Peristalsis begins after
swallow
Lower esophageal sphincter
(LES) controls release of
bolus into stomach
• Nitric oxide and VIP inhibit
closure (relax LES)
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Upper GI – A&P
• Stomach - Motility
Filling, storage, mixing, emptying
50 mL empty – stretches to 1000 mL
Pyloric sphincter
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Upper GI – A&P
• Stomach – Secretions
1-3 L of gastric juices
• Water, mucus, HCL, enzymes,
electrolytes
• Mucus protects lining of stomach
Chief cells - zymogen, pepsinogen,
gastric lipase
Parietal cells – HCL and intrinsic
factor
Cells in pylorus – histamine, gastrin,
somatostatin
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Upper GI – A&P
• Stomach – control of secretions
Acetylcholine, histamine, gastrin stimulate gastric secretions
Somatostatin - inhibits gastric
secretion
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© 2007 Thomson - Wadsworth
Upper GI – A&P
• Stomach – release of secretions
Phases:
• Cephalic - release of HCL and pepsinogen
stimulated by tasting, smelling, seeing
food
• Gastric - when food enters the stomach
• Intestinal - inhibitory; slows gastric
secretions and prepares small intestine
for receipt of acidic chyme
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© 2007 Thomson - Wadsworth
Upper GI – A&P
• Stomach – release of secretions
Inhibit action of chief and parietal
cells decreasing gastric juices
• CCK & secretin – slow gastric motility
• Somatostatin
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© 2007 Thomson - Wadsworth
Upper GI – A&P
• Stomach – Digestion & Absorption
Mechanical and chemical
HCL denatures protein structure and
converts pepsinogen to pepsin
Pepsin cleaves proteins
Absorption is limited except for
alcohol & aspirin
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Pathophysiology –
Oral Cavity
• Oral disease – can lead to nutritional
deficits
 Dental caries, periodontal disease
 Inflammatory conditions such as gingivitis,
stomatitis, glossitis, cheilosis
 Altered salivary gland function
• Xerostomia resulting from surgery or radiation or
blockage
• Sjogrens syndrome
• Dehydration
• Medications
© 2007 Thomson - Wadsworth
© 2007 Thomson - Wadsworth
© 2007 Thomson - Wadsworth
© 2007 Thomson - Wadsworth
Pathophysiology Oral Cavity
• Surgical procedures
Tongue, palate, pharynx
MMF – “wiring the jaw” – intake
limited to liquids and blenderized
foods
• Impaired taste (dysgeusia) or
ageusia
Chemotherapy, radiation, nervous
system diseases
Medications
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Pathophysiology Oral Cavity
• Nutrition Implications/Therapy
Inability to maintain oral intake,
difficulty swallowing
Texture modifications – soft, moist,
liquids, or blenderized
Increase kcal and protein density
• Modular supplements
• Liquid supplements
• Increase fat intake
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© 2007 Thomson - Wadsworth
Pathophysiology Oral Cavity
• Nutrition Therapy/Evaluation
Increase frequency of meals
Bland foods served at room temp.
Liberal use of fluids
Preference for cold and frozen foods
Oral hygiene
Monitor using food diary, observation,
or kcal count
Monitor weight gain or maintenance
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Pathophysiology Esophagus
• GERD - reflux of gastric contents
into the esophagus
Incompetence of LES
• Increased secretion of gastrin, estrogen,
progesterone
• Hiatal hernia
• Cigarette smoking
• Use of medications
• Foods high in fat, chocolate, spearmint,
peppermint, alcohol, caffeine
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Pathophysiology Esophagus
• GERD - symptoms
Dysphagia
Heartburn
Increased salivation
Belching
Pain radiating to back, neck, or jaw
Aspiration
Ulceration
Barrett’s esophagus
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Pathophysiology Esophagus
• GERD - Treatment
Medical management
Modify lifestyle factors
Medications – 5 classes – see Table
16.11
Surgery
• Fundoplication
• Stretta procedure
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© 2007 Thomson - Wadsworth
© 2007 Thomson - Wadsworth
Pathophysiology Esophagus
• GERD - Nutrition Therapy
Identify foods that worsen symptoms
Assess food intake esp. those that
reduce LES pressure, or increase
gastric acidity
Assess smoking and physical activity
Small, frequent meals
Weight loss if warranted
See Table 16.12
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Pathophysiology Esophagus
• Dysphagia – difficulty swallowing
Potential causes – see Table 16.13
Drooling, coughing, choking
Weight loss, generalized malnutrition
Aspiration to aspiration pneumonia
Treatment requires health care team
dg by bedside swallowing,
videofluoroscopy, barium swallow
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© 2007 Thomson - Wadsworth
Pathophysiology Esophagus
• Dysphagia – Nutrition Therapy
Use acceptable textures to develop
adequate menu
National Dysphagia Diet 1,2,3 – see
Table 16.15
Use of thickening agents and
specialized products
Monitor weight, hydration, and
nutritional parameters
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© 2007 Thomson - Wadsworth
© 2007 Thomson - Wadsworth
© 2007 Thomson - Wadsworth
Pathophysiology Esophagus
• Achalasia – motility disorder with
absence of peristalsis
Elevated LES pressure
Impaired relaxation of LES
Primary and secondary
Treatment includes medications and
invasive procedures
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© 2007 Thomson - Wadsworth
Pathophysiology Esophagus
• Achalasia – nutritional intervention
Dysphagia, vomiting, substernal pain
Body of esophagus loses muscle tone
causing it to stretch – poor oral
intake, weight loss
Texture modification
Increased kcal and protein density
Avoid extreme temp. or spicy foods
Small, more frequent meals
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Hiatal Hernia
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Pathophysiology Stomach
• Indigestion – dyspepsia
Abdominal pain, fullness, gas,
bloating, belching, nausea, reflux
• Nausea & Vomiting
Caused by drugs, toxins, metabolic
conditions, stress or extreme
emotions
Treat underlying cause
Medications or antiemetics
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Pathophysiology Stomach
• Severe Vomiting
Rupture
Hematemesis
Dehydration
Acid-base imbalances
Malnutrition
Aspiration pneumonia
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Pathophysiology Stomach
• Nausea & Vomiting – Nutrition
May lead to learned food aversions
Minimize symptoms and discomfort
See Table 16.18 for suggestions
Monitor hydration status
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© 2007 Thomson - Wadsworth
Pathophysiology Stomach
• Gastritis
 Inflammation of the gastric mucosa
 Primary cause: H. pylori bacteria
 Alcohol, food poisoning, NSAIDs
 Symptoms: belching, anorexia, abdominal
pain, vomiting
 Type A - automimmune
 Type B – H. pylori
 Increases with age, achlorhydria
 Treat with antibiotics and medications
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Pathophysiology Stomach
• Peptic ulcer disease - ulcerations of
the gastric mucosa that penetrate
submucosa
Gastric or duodenal
H. pylori
NSAIDS, alcohol, smoking
Certain foods, genetic link
Increased risk of gastric cancer
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Pathophysiology Stomach
• Peptic Ulcer Disease
Symptoms: epigastric pain relieved or
worsened by abdominal pain, burning
sensation
Relieved with eating or antacids
Rebound gastrin release – more pain
Presence of blood in the stool or
vomit
Treatment: triple/quadruple therapy
of meds, surgery
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Pathophysiology Stomach
• Peptic Ulcer Disease - Nutrition
Restrict only those foods known to
increase acid secretion
• Black and red pepper, caffeine, coffee,
alcohol, individually non-tolerated foods
Consider timing and size of meal
Do not lie down after meals
Small, frequent meals
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Pathophysiology Stomach
• Gastric Surgery
With complications: hemorrhage,
perforation, obstruction
Vagotomy
Vagotomy with pyloroplasty
Billroth I & II, Roux-en-Y
See Fig. 16.9
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© 2007 Thomson - Wadsworth
Pathophysiology Stomach
• Gastric Surgery - Nutrition
Implications
Reduced capacity
Changes in gastric emptying & transit
time
Components of digestion altered or
lost
Decreased oral intake, maldigestion,
malabsorption
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Pathophysiology Stomach
• Gastric Surgery - Dumping
Syndrome
Increased osmolar load enters small
intestine too quickly from stomach
Release of hormones, enzymes, other
secretions altered
Food “dumps” into small intestine
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© 2007 Thomson - Wadsworth
Pathophysiology Stomach
• Gastric Surgery - Dumping
Syndrome
Early dumping – 10-20 min.;
diarrhea, dizziness, weakness,
tachycardia
Intermediate - 20-30 min.;
fermentation of bacteria produces
gas, abdominal pain, etc.
Late dumping - 1-3 hrs.;
hypoglycemia
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Pathophysiology Stomach
• Gastric Surgery - Dumping
Syndrome
Other nutritional concerns: vitamin
and mineral deficiencies, lack of
intrinsic factor, iron deficiency,
osteoporosis
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Pathophysiology Stomach
• Dumping Syndrome - Nutrition
 “Anti-dumping” diet
 Slightly higher in protein & fat
 Avoid simple sugars & lactose
 Calcium & vitamin D
 Liquid between meals
 Small, frequent meals
 Lie down after meals
 Assess for weight loss, malabsorption, and
steatorrhea
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© 2007 Thomson - Wadsworth
Other Conditions
• Stress ulcers
Caused by sepsis, shock, burns, head
injuries
Infusion of H2 blockers, liquid
antacids
• Zollinger-Ellison syndrome
Gastric acid hypersecretion
Symptoms similar to PUD but
unresponsive to therapy
© 2007 Thomson - Wadsworth