Nutrient Intake, Digestion, Absorption, and Excretion Flashcards

1
Q

Which cells in the GI tract secrete more than 30 GI hormone peptides?

A

Neuroendocrine cells

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2
Q

What are the major inputs influencing appetite regulation?

A

Short term signals related to meal ingestion that are transmitted by the “gut-brain” axis
Signals associated with energy stores that are mediated by leptin
Signals deriving from lean body mass
Circadian rhythm

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3
Q

What is the major orexigenic (appetite stimulating) gut hormone?

A

Ghrelin

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4
Q

Name anorexigenic (appetite suppressing) gut hormones

A

Glucagon-like peptide-1 and -2 (GLP-1, GLP-2)
Oxyntomodulin (OXM)
Peptide tyrosine-tyrosine (PYY)
Pancreatic polypeptide (PP)
Cholecystokinin (CCK)

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5
Q

How are gut- and fat-derived hormones (ghrelin, leptin, insulin, and PYY) involved in feedback regulation of feeding?

A

Through signals affecting hunger, satiety, and energy needs

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6
Q

How does ghrelin increase food intake?

A

By stimulating the ARC of the hypothalamus

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7
Q

Where in the brain are neural and hormonal signals that influence food intake located?

A

The arcuate nucleus (ARC) of the hypothalamus and the brainstem

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8
Q

Name the site of secretion, stimulating factors, mechanism of action, and effect of GLP-1 (glucagon-like peptide-1)

A

Distal gut
Stimulated by food intake proportional to energy intake
Works by binding GLP-1 receptors in pancreatic islet cells, heart, lungs, and brain (ARC and PVC)
Reduces appetite and energy intake; delays gastric emptying; enhances postprandial insulin release

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9
Q

Name the site of secretion, stimulating factors, mechanism of action, and effect of OXM (oxyntomodulin)

A

L cells of the distal gut
Stimulated by food intake
Works as agonist at glucagon receptor; has undefined neural effects
Reduces food intake; increases energy expenditure

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10
Q

Name the site of secretion, stimulating factors, mechanism of action, and effect of PYY (peptide-tyrosine-tyrosine)

A

L cells of the distal gut
Stimulated by food intake (released in proportion to energy, fat, and protein intake)
Mechanism of action: Y receptors found throughout the CNS and on vagal afferents, NPY (neuropeptide Y) inhibition, POMC (proopiomelanocortin) activation, associated with increased activity of OFC (orbitofrontal cortex)
Reduces food intake

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11
Q

Name the site of secretion, stimulating factors, mechanism of action, and effect of PP (pancreatic polypeptide)

A

Pancreatic polypeptide cells of the islets of Langerhans in the pancreas
Stimulated by food intake and vagal stimulation
Enters CNS via diffusion in the brain stem and ARC
Reduces food intake

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12
Q

Name the site of secretion, stimulating factors, mechanism of action, and effect of CCK (cholecystokinin)

A

L cells of the gut, nerves in distal ileum and colon, neurons in the brain
Stimulated by dietary protein and fat, gastric acid
Reduces hypothalamic NPY (neuropeptide Y)
Inhibits gastric emptying and reduces food intake

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13
Q

Name the site of secretion, stimulating factors, mechanism of action, and effect of Leptin

A

Large amounts from the gastric mucosa; white adipose tissue
Food deprivation is associated with low levels
Low levels influence ARC; possibly decreases gene expression of NPY and increases activity of POMC-secreting neurons
Low levels increase energy intake and decrease energy expenditure

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14
Q

Name the site of secretion, stimulating factors, mechanism of action, and effect of Ghrelin

A

Stomach
Food intake decreases levels; fasting increases levels
Stimulates ARC via receptors; stimulated GH secretion
Increases food intake

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15
Q

Describe the role of fiber (especially resistant starch R2) on the feeding response

A

It has satiety value with associated decreases in food intake

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16
Q

True or false: stomach size can influence the amount of food eaten

A

True. Its size is related to the amount of food habitually eaten.

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17
Q

How is aging associated with decreased appetite and food intake

A

Likely because of decreased basal hunger rather than increased meal satiety

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18
Q

Name some adverse effects that have been associated with megestrol

A

Nausea, vomiting, gas, diarrhea

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19
Q

GI muscle fibers are depolarized (contraction of the muscle) in response to?

A

Stretching of the muscle fiber
Acetylcholine released by parasympathetic neurons
Gut hormones

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20
Q

Inhibition of GI muscle contraction is associated with a hyperpolarized state which is caused by?

A

Norepinephrine or epinephrine
Sympathetic nerves that secrete norepinephrine

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21
Q

How is the enteric nervous system connected to the central nervous system?

A

By parasympathetic fibers (stimulates motility) and sympathetic fibers (modulates activity of ENS with inhibitory signals)

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22
Q

Factors that regulate gastric emptying

A

Volume of food
Gastrin
Enteric gastric nervous reflexes from the duodenum
Ghrelin
Hormonal feedback from the duodenum

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23
Q

What are the neurotransmitters of the ENS?

A

Acetylcholine
Norepinephrine and serotonin
y-aminobutyrate
Adenosine triphosphate (ATP)
Nitric oxide (NO) and carbon monoxide (CO)
Dopamine
CCK
Substance P
Vasoactive intestinal peptide (VIP)
Somatostatin
Leu-enkephalin
Met-enkaphalin

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24
Q

What are some sensory stimuli in the ENS that are involved in the neural control of the gut?

A

Irritation of the mucosa, excessive distention, or chemical stimuli

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25
Q

Describe the stimuli for secretion, site of secretion and action of gastrin for GI motility

A

Stimuli are protein, GI distention, gastric-releasing peptide
Secreted by G cells of the antrum, duodenum, and jejunum
Stimulates gastric acid secretion and mucosal growth; promotes gastric emptying

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26
Q

Describe the stimuli for secretion, site of secretion, and action of cholecystokinin for GI motility

A

Stimuli are protein, fat, and acid
Secreted by I cells of the duodenum, jejunum, and ileum
Stimulates pancreatic enzyme secretion, gallbladder contraction, and growth of exocrine pancreas; inhibits gastric emptying

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27
Q

Describe the stimuli for secretion, site of secretion, and action of secretin for GI motility

A

Stimulus is acid
Secreted by S cells of the duodenum, jejunum, and ileum
Stimulates pepsin, pancreatic and biliary bicarbonate secretion, and growth of exocrine pancreas; inhibits gastric emptying and gastric acid secretion

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28
Q

Describe the stimuli for secretion, site of secretion, and action of gastric inhibitory peptide (GIP) for GI motility

A

Stimuli are protein, fat, carbohydrate
Secreted by K cells of the duodenum and jejunum
Stimulates insulin release and secretion; inhibits gastric acid secretion and emptying

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29
Q

Describe the stimuli for secretion, site of secretion, and action of motilin for GI motility

A

Stimuli are fat, acid, gastric distention, bile acids, serotonin, and low pH in duodenum
Secreted by M cells of the duodenum and jejunum, stomach, colon
Stimulates gastric motility and intestinal motility

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30
Q

Describe the stimuli for secretion, site of secretion, and action of vasoactive intestinal peptide (VIP) for GI motility

A

Stimulus is GI distention
Secreted by nerves of the GI tract
Stimulates secretion of electrolytes and water secretion; inhibits gastric acid

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31
Q

Describe the stimuli for secretion, site of secretion, and action of somatostatin for GI motility

A

Stimulus is acid
Secreted by pancreas, GI mucosa, hypothalamus
Inhibits secretion of gastrin, VIP, GIP, secretin, motilin, exocrine pancreatic secretion, gallbladder contraction, gastric acid secretion, and gastric motility

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32
Q

Describe the stimuli for secretion, site of secretion, and action of serotonin (5-HT) for GI motility

A

Stimuli are luminal contents including glucose and SCFAs, GI distention
Secreted by nerve fibers of the enteric nervous system
Increases intestinal motility

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33
Q

Describe the stimuli for secretion, site of secretion, and action of peptide-tyrosine-tyrosine (PYY) for GI motility

A

Stimulus is fat
Secreted by jejunum
Inhibits gastric acid secretion and gastric motility

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34
Q

What motor functions of the stomach contribute to digestion?

A

Storing food, mixing food with gastric secretions, and emptying the semifluid mixture (chyme) into the duodenum

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35
Q

What factors decrease gastric tone?

A

Duodenal distention, colonic distention, ileal perfusion with glucose

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36
Q

The inhibitory reflexes of the duodenum are stimulated by what 5 factors?

A
  1. duodenal distention
  2. irritation of the duodenal mucosa
  3. pH less than 3.5 or 4.0
  4. high osmolality
  5. the presence of breakdown products of protein and fat digestion
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37
Q

Which macronutrient is the strongest stimulus for hormones of the duodenum and jejunum?

A

Dietary fat

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38
Q

The tone of which portions of the stomach influence liquid and solid emptying?

A

Proximal stomach influences liquid emptying
Distal stomach is involved in solid emptying

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39
Q

What is the average half-emptying time of water or isotonic saline?

A

12 minutes
Example: if one drinks 300 ml of water, 150 ml will enter the duodenum in about 12 minutes

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40
Q

What factors regulate liquid emptying?

A

Duodenal osmoreceptors, secretin, and VIP

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41
Q

What is the half-emptying time of solids?

A

45-110 minutes

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42
Q

Intragastric pressure ____ in response to the swallowing reflex and in response to gastric distention by the presence of food

A

Falls

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43
Q

What is the volume that a relaxed stomach can hold?

A

0.8 to 1.5 L

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44
Q

What factors influence the rate of gastric emptying time of solids?

A

Meal particle size, energy content, and fat content

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45
Q

When the swallowing mechanism is bypassed, such as in NG feeding, the rate of gastric emptying is ______.

A

Faster

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46
Q

Why would gastric emptying time decrease if feeding tubes are placed in the jejunum, bypassing the duodenum?

A

The duodenal mucosa possesses sensory receptors that are associated with neurohormonal reflexes that influence gastric emptying time

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47
Q

What factors determine the amount of chyme that enters the intestine from the stomach?

A

Duodenal distention, acidity, osmolar changes, and the presence of products of carbohydrate, protein, and fat digestion

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48
Q

When are segmentation contractions (mixing contractions) of the small intestine elicited?

A

When the small intestine is distended by chyme

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49
Q

What is the average time it takes for chyme to travel from the pylorus to the ileocecal valve?

A

3-5 hours. The rate of mixing contractions is 2-3 per minute or maximally 12 per minute. Propulsive movements of the small intestine (peristalsis) move in the direction of the anus at a rate of 0.5-2.0 cm/second.

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50
Q

When is neural control partly initiated during intestinal peristalsis?

A

When chyme stretches the intestinal wall

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51
Q

What are the stimulatory hormones of intestinal peristalsis?

A

Gastrin, CCK, insulin, motilin, and serotonin

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52
Q

What is the volume of chyme that empties into the cecum?

A

1500-2000 ml/day

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53
Q

What is the purpose of the ileocecal valve?

A

To prevent backflow of fecal content into the small intestine

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54
Q

How long does it take for chyme to move from the ileocecal valve through the colon?

A

8-15 hours

55
Q

On average, after abdominal surgery, the small intestine regains peristalsis within ____ hours (or sooner), and motility of the stomach and colon returns between ____ and ____ hours

A

24, 48, 72

56
Q

In a previously well-nourished patient, parenteral nutrition should only be considered after how many days of NPO?

A

7 days. PN has been associated with higher infection morbidity in previously well-nourished patients compared with standard care

57
Q

Aside from abdominal surgery, what other conditions/situations can cause ileus?

A

Infection, inflammation, electrolyte imbalance, the use of certain drugs such as sedatives, opioid analgesics, a2-adrenergic receptor agonists, catecholamine vasopressors

58
Q

Name potential etiologies or contributing factors of ileus?

A

Opiate use, sympathetic hyperactivity, altered spinal-intestinal neural reflexes, changes in hormone expression and secretion, hypomagnesemia, hypokalemia, and local and systemic inflammation

59
Q

What is chronic intestinal pseudo-obstruction (CIP)?

A

A motility disorder of peristalsis that most often affects the small bowel but can occur at any point in the GI tract

60
Q

Name the secondary causes of CIP

A

Collagen vascular and endocrine diseases, neurological diseases, medication-related effects

61
Q

Describe the treatment plan for CIP

A

Palliation of symptoms including nausea and vomiting with antiemetics and/or prokinetics, provision of IV hydration or PN, nocturnal cyclic EN when possible, and, when necessary, withholding of oral intake of food

62
Q

What is the preferred mode of nutrition for CIP?

A

Oral

63
Q

Describe the MNT for CIP patients who can consume an oral diet

A

Recommend small, frequent meals low in fat and fiber, with an emphasis on liquid forms of energy and protein. Daily multivitamin and mineral supplement is recommended, and if the patient has small intestinal bacterial overgrowth (SIBO), emphasis should be placed on fat-soluble and B12 vitamins.

64
Q

List serious consequences of diarrhea

A

Severe fluid and electrolyte abnormalities; fluid loss, dehydration, hypovolemia; hypovolemic shock and cardiovascular collapse; increased risk of pressure ulcers, compromised nutrition status, increase hospital LOS

65
Q

What percent of cases of antibiotic-associated diarrhea (AAD) is from C. difficile infection?

A

20%

66
Q

What is the standard recipe for oral rehydration solution published by the World Health Organization?

A

2.6 gm NaCl, 13.5 gm anhydrous glucose, 1.5 gm potassium chloride, 2.9 gm trisodium citrate, and 1 L water

67
Q

What MNT should be offered to a patient who has reobstruction of the small intestine after surgery (lysis of adhesions) for small bowel obstruction?

A

If the patient has a normal nutrition status on admission, the best nutrition intervention is no initial intervention. Would keep patient NPO on bowel rest and evaluate for PN on hospital day 7

68
Q

What enteral MNT would you offer to a patient with severe diarrhea related to C.diff pseudomembranous colitis (PMC)?

A

Evidence-based diet recommendations for PMC diarrhea have not been established, however the goal is to initiate nutrition through the GI tract as early as possible to limit gut mucosa atrophy. Would keep patient NPO until diarrhea improves of antibiotic therapy, then initiate on caffeine-free clear liquids, and then advance to low-lactose, low-fat, low-fiber diet. Supplemental fiber use in C.diff diarrhea is not supported by ASPEN. IV fluids if oral intake does not keep up with losses. PN should not be offered unless patient presents severely malnourished.

69
Q

How do SCFAs help control diarrhea?

A

By stimulating the uptake of water and electrolytes by colonocytes

70
Q

Name some causes of gastroparesis

A

Diabetes mellitus (at least 25% of cases), complications of surgery, renal disease, collagen disease, drugs, malignancy, hypothyroidism, and possible idiopathic reasons

71
Q

What surgical intervention can be offered for a patient who fails medical treatment for gastroparesis?

A

A near-total gastrectomy and Roux-en-Y gastrojejunostomy.

72
Q

What are the dietary treatments for gastroparesis?

A

Small, frequent meals, drinking fluids with meals, limiting dietary fat and fiber, maintaining good glucose control, and, when necessary, feeding past the pylorus

73
Q

What nutrition intervention is recommended for a patient with gastroparesis who has failed to respond to dietary intervention?

A

Jejunostomy-tube placement for long-term intestinal feedings and oral diet of small amounts of low-fat, low-fiber foods with liquids as tolerated (to address the psychosocial need to eat). If patient is receiving nighttime cyclic feedings, may also need to change to a longer-acting insulin to control glucose levels during nighttime feeding. Jejunal feedings bypass the stomach and obviate the potential of formula intolerance associated with delayed gastric emptying.

74
Q

Name conditions associated with constipation

A

Diabetes mellitus, hypothyroidism, hypercalcemia, dehydration, neurologic disorders, anorectal disease, and collagen vascular/muscular diseases

75
Q

What are the first-line medication treatments for constipation when nonpharmacological approaches fail? Second-line?

A

First-line: Hydrophilic colloids (psyllium, bran methylcellulose, polycarbophil), stool softeners, osmotic laxatives (polyethylene glycol, lactulose, sorbitol, and magnesium salts).
Second-line: Stimulants (senna/docusate, bisacodyl/docusate, or casanthranol/docusate) and lubricants (mineral oil).

76
Q

What is the disadvantage of using mineral oil for constipation?

A

It binds fat-soluble vitamins and, if aspiration occurs, could cause a lipoid pneumonia.

77
Q

What is dumping syndrome?

A

A group of symptoms that develop after gastric surgery and are related to increased gastric emptying following vagotomy and bypass or destruction of the pylorus. Can also occur with too rapid infusion of EN through a small-bore feeding tube. It is accompanied by both GI symptoms and vasomotor symptoms.

78
Q

What are the GI and vasomotor symptoms of dumping syndrome?

A

GI symptoms: feeling of fullness after eating, crampy abdominal pain, nausea, vomiting, and explosive diarrhea
Vasomotor symptoms: diaphoresis, weakness, dizziness, flushing, and palpitations

79
Q

What are the time frames for early vs late dumping?

A

Early: within 30-60 minutes of eating
Late: occurs 2-3 hours after eating and is limited to vasomotor symptoms

80
Q

What is the cause of the GI and vasomotor symptoms of dumping syndrome?

A

GI: related to the rapid emptying of hyperosmolar chyme into the small intestine from the stomach, eliciting an osmotic diuresis into the intestinal lumen and subsequent distention
Vasomotor: rapid delivery of glucose to the upper small intestine, which results in peripheral and splanchnic vasodilation. This rapid delivery precipitates and increased serum insulin release followed by hypoglycemia and vasomotor symptoms

81
Q

What is the dietary treatment for dumping syndrome?

A

Involves slow introduction of solid food, elimination of simple sugars, frequent small meals, and no liquids with meals. Patients are advised to lie down after eating and consider adding functional fibers to delay gastric emptying. The initial post-op period should not include simple sugars. Dairy products should be restricted initially because temporary lactose intolerance may occur. Liquid multivitamin/mineral supplements and vitamin B12 injections may be warranted in patients who have undergone a gastric resection.

82
Q

What are the 2 primary functions of secretions in the GI tract?

A

To supply digestive enzymes and to supply lubricating mucus

83
Q

What populations are at risk for xerostomia?

A

Obese patients, older adults, patient’s with Sjogren’s syndrome, those undergoing radiotherapy or chemotherapy for cancer, those with hormone disorders and infections

84
Q

What are some consequences of hyposalivation?

A

Alterations in taste perception, chewing and swallowing problems, intolerance of spicy foods, can encourage dietary choices that compromise nutrition status and increase the risk for dental plaque and periodontal disease

85
Q

How does hyposalivation occur with obesity?

A

Via increased leptin and decreased ghrelin

86
Q

What are the contents of saliva?

A

Mucin (for lubrication), ptyalin (alpha-amylase; enzyme for starch digestion), immunoglobulin A (IgA), lysozyme (for protection against oral bacteria), components that play a role in innate immunity

87
Q

How much saliva do humans secrete each day?

A

Approximately 1000-1500 ml/day

88
Q

Where do gastric secretions derive from?

A

Mucus-secreting cells, oxyntic glands (gastric glands), and pyloric glands

89
Q

What 3 cells make up oxyntic glands?

A

Mucus-producing cells, peptic (chief) cells, and parietal cells

90
Q

Peptic cells secrete ___ and ___; parietal cells secrete ___ and ___.

A

Pepsinogen and gastric lipase
Hydrogen chloride (HCl) and intrinsic factor

91
Q

What is the pH of the gastric acid?

A

Approximately 0.8

92
Q

What is a possible consequence of the destruction of parietal cells, such as with chronic gastritis?

A

Achlorhydria (the absence of acid) develops in addition to pernicious anemia and vitamin B12 deficiency caused by loss of intrinsic factor. Intrinsic factor is required for the absorption of vitamin B12 and is secreted by the same cells that secrete HCl

93
Q

What are the biochemical stimulants for acid secretion?

A

Gastrin, histamine via H2 receptors, and acetylcholine released by parasympathetic stimulation

94
Q

Gastrin is secreted in response to the presence of ___

A

Luminal oligopeptides (peptide products of protein digestion), gastric distention, and GRP (bombesin)

95
Q

The presence of carbohydrate, protein, or fat in the duodenum ____ gastric acid and pepsin secretion as well as gastric motility

A

Inhibits

96
Q

Caffeine and alcohol ____ gastrin and acid production

A

Stimulate

97
Q

Peptic ulcers develop when ____ is compromised

A

The gastric lining’s protective barrier against irritation and autodigestion

98
Q

What is the treatment for peptic ulcers?

A

Suppression of gastric acid production, ie. Proton-pump inhibitors (exert their effects on acid suppression by interfering with hydrogen potassium ATP activity), H2-receptor antagonist drugs (block histamine stimulation of acid production)

99
Q

What are the 3 phases in which gastric juice is secreted?

A
  1. Cephalic phase
  2. Gastric phase
  3. Intestinal phase
100
Q

Describe the cephalic phase of gastric juice secretion

A

Acid is secreted via vagal stimulation in response to the sight, smell, and/or taste of food. Vagus nerve releases acetylcholine (stimulates ECL cells and parietal cells). Accounts for 30% of the volume of acid secretion.

101
Q

Describe the gastric phase of gastric juice secretion

A

Begins when food arrives in the stomach. Amino acids and peptides stimulate the G cells in the antrum to produce gastrin (enters the general circulation and stimulates parietal cells as an endocrine hormone). Gastric distention also leads to acid secretion via a reflex involving the vagus nerve. Accounts for 60% of the volume of acid secretion.

102
Q

Describe the intestinal phase of gastric juice secretion

A

Food in the duodenum continues to stimulate small amounts of gastric secretions (likely related to the small amount of gastrin that is secreted by the duodenal mucosa). Accounts for approximately 10% of gastric acid secretion.

103
Q

Describe the multiple ways in which gastric secretions are inhibited by signals from the intestines

A

Food in the small intestine stimulate gastrin release and initiates a reverse enterogastric reflex that inhibits gastric secretions. The presence of acid, fat, products of protein digestion, hyper- or hypotonic fluids, or irritants in the proximal small bowel stimulate the secretions of gastric secretion-inhibiting hormones (secretin, GIP, VIP, somatostatin). The presence of carb, protein, or fat in the duodenum inhibits gastric acid and pepsin secretion and gastric motility.

104
Q

What are the components of bile?

A

Water, bile salts, bile pigments, cholesterol, lecithin, fatty acids, and electrolytes

105
Q

What are the two principal bile acids?

A

Cholic acid and chenodeoxycholic acid

106
Q

What are the secondary bile acids that are converted by colonic bacteria?

A

Cholic acid converts to deoxycholic acid
Chenodeoxycholic acid converts to lithocholic acid

107
Q

What are the bile pigments?

A

Bilirubin and biliverdin

108
Q

Describe jaundice and how it can be detected

A

Jaundice occurs in pathological conditions when bilirubin accumulates in the blood, skin, sclera, and mucous membranes. It imparts a yellow color and can be detected when total plasma bilirubin exceeds 2 mg/dL

109
Q

Bile production is stimulated by ___ and ___

A

The vagus nerve and secretin

110
Q

What is the sphincter of Oddi?

A

The exit of the common bile duct into the duodenum. It remains closed between meals, directing bile to the gallbladder. It relaxes (opens) after a meal (especially if it is high in fat) when the gallbladder contracts. Relaxation of the sphincter is mediated by the action of CCK

111
Q

How much bile is secreted per day?

A

Approximately 500 mL

112
Q

What is enterohepatic circulation?

A

Reabsorbed bile salts (90-95% of which are reabsorbed in the terminal ileum) and bile pigments are transported to the liver via the portal vein and then are reexcreted in the bile

113
Q

What is the role of bile salts in the digestion of fat?

A

To act as emulsifiers along with phospholipids and monoglycerides

114
Q

In the fasting state without any EN, gastric secretions can amount to ___ to ___ mL/day, and biliary and pancreatic secretions can be up to ____ to ____ mL/day.

A

500-1000 mL/day
1000-2000 mL/day

115
Q

When colonic pressure increases, the ileocecal valve ____. When ileal pressure increases or when food exits the stomach, the ileocecal valve ___.

A

Shuts
Opens

116
Q

Brunner glands secrete ___

A

Mucus, to protect the duodenum from gastric acid

117
Q

Pancreatic secretions, intestinal secretions, and bile neutralize gastric acid to raise the pH of duodenal contents to ___

A

6-7

118
Q

Name the pancreatic enzymes found in pancreatic juice

A

Carbohydrate - pancreatic amylase
Protein - pancreatic proteases (trypsin, chymotripsin, carboxypolypeptidase, proelastase, collagenase)
Fat - pancreatic lipase, cholesterol esterase, phospholipase

119
Q

Why do oral rehydration solutions used to treat Na+ and water losses from diarrhea contain NaCl and glucose?

A

Na+ facilitates the absorption of glucose, some amino acids, and bile acids

120
Q

What percent of dietary iron is absorbed under conditions of iron deficiency?

A

3-6%

121
Q

Iron absorption is inhibited by:

A

Phytates in cereal, phosphates, and oxalates. These compounds for insoluble compounds with iron

122
Q

Does the passage of feces continue during prolonged bowel rest when patients are restricted from consuming food?

A

Yes, fecal contents include material other than food residue. Feces contains bacteria (comprises 30% of the dry weight of fecal matter), inorganic material, fiber, water, sloughed off undifferentiated stem cells

123
Q

How are medium-chain triglycerides absorbed?

A

MCTs are water soluble, they do not require the formation of micelles or the action of bile salts. MCTs are hydrolyzed and pass through enterocytes directly into the portal circulation. MCTs may be used as an energy supplement in patients who maldigest or malabsorb fat

124
Q

What percent of cardiac output is delivered to the splanchnic circulation at rest?

A

25%

125
Q

What percent of total body oxygen is consumed at rest by the splanchnic organs?

A

30%

126
Q

During feeding, splanchnic blood flow increases __% to __% and oxygen demand in the splanchnic-supplied organs increases up to __%

A

40% to 60%
30%

127
Q

Where does all blood in the GI tract, including the spleen and pancreas, flow to?

A

To the liver via the portal vein

128
Q

What is the reticuloendothelial system?

A

A system of macrophages that clears the blood of bacteria and other particulate matter to prevent systemic infection before blood leaves the liver. In the liver, blood encounters RED cells in the lining of sinusoids (liver blood cells).

129
Q

Name the arteries that supply blood to the small intestine. The stomach?

A

Superior and inferior mesenteric arteries (branch off the aorta) for the small intestine. Celiac artery for the stomach.

130
Q

When does mucosal atrophy occur?

A

During starvation, stress, PN, and bowel rest

131
Q

True or false: the bowel mucosa requires luminal nutrients to supply its nutrient needs

A

True. After 1 week of a protein-deficient diet, the microvilli shorten

132
Q

What is the principal metabolic fuel for intestinal cells?

A

Glutamine. Its absence may directly contribute to mucosal atrophy that accompanies bowel rest.

133
Q

When should EN be withheld in patients with hypoperfused gut?

A

When patients are being initiated on catecholamines, when catecholamine doses are increasing, or when patients require a high level of hemodynamic support including high-dose catecholamines (norepinephrine, epinephrine, dopamine) to maintain cellular perfusion.