Ch 1: Nutrient Intake, Digestion, Absorption, & Excretion Flashcards

1
Q

Major inputs influencing appetite regulation include:

A
  • Short term signals r/t meal ingestion transmitted by th gut-brain axis
  • Signals associated with the energy stores that are mediated by leptin
  • Signals deriving from LBM
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2
Q

What part of the brain regulates appetite?

A

Hypothalamus

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3
Q

What is the adipose tissue-derived hormone that acts on the hypothalamus to decrease PO intake and increase energy expenditure?

A

Leptin

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4
Q

What type of meals should be initiated to increase nutrient intake during nutrition rehabilitation of undernourished patients?

A

small frequent meals

Stomach size impacts PO intakes

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5
Q

Products of what macronutrient are shown to influence development of nausea?

A

fat digestion

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6
Q

What stimulates peristaltic waves in esophagus and gastric emptying?

A

vagus nerve

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7
Q

When the swallowing mechanism is bypassed (ex: NG feeds), the rate of gastric emptying is

faster or slower?

A

faster

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8
Q

Volume of chyme that empties into the cecum is

A

1500-2000 mL/d

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9
Q

Consistency of stool in ascending colostomies vs descending colostomies

A
  • Ascending colon – receives liquid contents
  • Transverse colon → descending colon: luminal contents become more solid
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10
Q

What is the rectal relaxation and subsequent urge to defecate 2/2 gastric distention by food called?

A

Gastrocolic reflex

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11
Q

Why type of motility is the last to recover following GI surgery?

A

Colon motility

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12
Q

MNT post-op management SBO

A

When feasible, provide PO/EN postop within 24 hours of surgery for optimal patient outcomes
* Failure to initiate EN in the immediate post-op period can delay return of bowel function

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13
Q

Why can EN can be initiated as soon as 6 hours after surgery?

A

EN can be initiated within 6 hours after surgery because motility returns quickly in the small bowel

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14
Q

What is Chronic Intestinal Pseudo-Obstruction (CIP)?

A

Motility disorder of peristalsis

  • Most often affects small bowel, but can occur at any point in the GI tract
  • Mechanical obstruction is absent, but presence of massively dilated bowel can prevent normal function
  • Colonic pseudo-obstructions – complication of narcotic use, bed rest, or disease
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15
Q

Chronic Intestinal Pseudo-Obstruction (CIP)

MNT for CIP

A
  • Small, frequent meals
  • Emphasis on liquid forms of energy/protein
  • MVI with minerals
  • Consider elemental diets with MCTs if patient doesn’t tolerate polymeric nutrients
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16
Q

Chronic Intestinal Pseudo-Obstruction (CIP)

If patient has SIBO in CIP

A

add fat-soluble and B12 vitamins

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17
Q

Definitition of Diarrhea

A

2-3 liquid stools or >250 mL liquid stool/day

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18
Q

What losses occur with diarrhea?

A

Losses of sodium, potassium, and water

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19
Q

When evaluating diarrhea:

Labs and etiology

A
  • Infectious process – a left shift with increased WBC
  • Anemia – decreased Hgb from blood loss
  • Dehydration – increased (s)Na and BUN
  • Losses – decreased (s)Na and (s)K
  • Acidosis – d/t hyperchloremia
  • Alkalosis – d/t dehydration
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20
Q

Pseudomembranous colitis (PMC):

A
  • intestinal inflammation in the colon
  • The bacterium that causes PMC is Clostridium difficile
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21
Q

Why do you not want to use antiperistaltic agents with infectious diarrhea?

A

Slowing GI motility in setting of infectious diarrhea may increase the risk of bacterial translocation

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22
Q

MNT for PMC diarrhea

A

Evidenced-based diet recommendations for PMC diarrhea haven’t been established

Anecdotal MNT:
Clear liquids (caffeine free) → low lactose/fat/fiber diet
* Caffeine/stimulatory effects on GI motility
* Solids - addresses likely transient nutrient intolerances associated with suspected loss of brush border enzymes r/t diarrhea

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23
Q

Do ASPEN guidelines support the use of supplemental fiber in patients with Cdiff?

A

No

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24
Q

What patient population can receive soluble fermentable fiber in standard EN formulas?

A

Hemodynamically stable patients with noninfectious diarrhea

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25
Q

How do SCFAs help to control diarrhea?

A

By stimulating uptake of water and electrolytes by colonocytes

Colonic bacteria ferment fibers (FOS, inulin, pectin, guar gum, psyllium) to SCFAs.

SCFAs (esp Butyrate) are major energy sources for colonocytes

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26
Q

What patient population should not receive insoluble fiber?

A

Critically ill

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27
Q

What patient population should not receive any form of fiber (soluble or insoluble)?

A

Patients at risk for bowel ischemia

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28
Q

MNT for gastroparesis

A
  • small, frequent meals;
  • drinking fluids with meals;
  • limiting dietary fat and fiber;
  • maintain good glucose control.
  • When necessary, feed past the pylorus
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29
Q

MNT for dumping syndrome

A
  • slow reintroduction of solid food
  • no simple sugars
  • frequent small meals
  • no liquids with meals

can try fiber to delay gastric emptying

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30
Q

What secretes saliva and how much do you excrete in a day?

A
  • Secreted by parotid, submandibular, and sublingual glands
  • Excrete 1000-1500 mL/d
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31
Q

What does saliva include?

A
  • mucin for lubrication
  • ptyalin (a-amylase; aka salivary amylase) - enzyme for starch digestion
  • immunoglobulin A (IgA) and lysozyme for protection against oral bacteria
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32
Q

Hyposalivation

A
  • Often occurs in obesity via increased leptin and decreased ghrelin
  • Can lead to alterations in taste perception, chewing/swallowing problems, intolerance of spicy foods
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33
Q

Daily amount of gastric secretions:

A

2500 mL/d

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34
Q

What do the Parietal cells of the stomach secrete?

A

HCl and Intrinsic Factor

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35
Q

What do the Peptic (or chief) cells secrete?

A

pepsinogen and gastric lipase

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36
Q

Why do oxyntic glands secrete mucus?

A

To protect the gastric lining and duodenum from HCl

37
Q

What happens when parietal cells are destroyed?

A

Destruction of parietal cells (ex: chronic gastritis) → development of

  • achlorhydria (absence of acid)
  • pernicious anemia
  • B12 deficiency
38
Q

What stimulates gastrin and acid production?

A

Caffeine and alcohol

39
Q

Proton pump inhibitor

A

Interfere with H,K-ATP activity

40
Q

H2-receptor antagonist

A

block histamine stimulation of acid production

41
Q

Why do peptic ulcers develop and what meds are prescribed for management?

A
  • Develop when gastric lining’s protective barrier against irritation/autodigestion is compromised
  • PPI & H2 receptor antagonist
42
Q

Function of bile

A

Central to fat digestion and absorption
* Emulsifier (bile salts)
* Aids absorption of digested fats into intestinal mucosa

43
Q

Bile salts - how much does the body reabsorb per day?

A

90-95% reabsorbed in the terminal ileum

44
Q

What do white stools mean?

A

bile acids are prevented from entering the colon (ex: biliary obstruction)

45
Q

How many mL of alkaline, bicarbonate rich pancreatic juice is secreted daily into the duodenum via the sphincter of Oddi per day?

A

1500 mL/d

46
Q

In normal circumstance the pancreas releases small amounts of enzymes into blood circulation. During acute pancreatitis, serum levels of what enzymes rise dramatically?

A

amylase and lipase

47
Q

Fasted state without EN – peristalsis still occurs, even when NPO

gastric, biliary, pancreatic secretion amounts

A
  • Gastric secretions: 500-1000 mL/d
  • Biliary and pancreatic secretions: 1000-2000 mL/d
48
Q

Composition of the chyme partially determines the composition of pancreatic juice

Pancreatic juice contains enzymes for 3 major macronutrients:

A
  • CHO – pancreatic amylase
  • Protein – pancreatic proteases
  • Lipids – pancreatic lipase, cholesterol esterase, and phospholipase
49
Q

What is the length of the small bowel?

A

can vary from 12-20 feet
(350-600 cm)

50
Q

small bowel

Brush border

A

microvilli on the edge of the epithelium of the villi that is specialized for absorption

51
Q

small bowel

Enterocytes

A
  • a mucosal cell of the intestinal lining
  • role in digestion is ensuring the uptake of ions, water, nutrients, vitamins and absorption of unconjugated bile salts
52
Q

small bowel turnover

The loss of sloughed cells = how many grams of protein loss?

A

30g protein/day loss

53
Q

Purpose of mucus in the colon

A

provides an adherent medium to hold feces together

54
Q

Digestion of Starch

A
  1. Mouth – salivary a-amylase
  2. Stomach – salivary amylase inhibited by gastric acid
  3. Small bowel – pancreatic a-amylase
  4. Brush border enzymes – further digestion of oligosaccharides
55
Q

Deficiency of lactase enzyme is common in which populations?

A
  • African Americans
  • Native Americans
  • Asians
  • Individuals of Mediterranean descent
56
Q

Acquired disorders of brush-border enzyme deficiency is

A
  • Usually transient and resolves in a short period of time
  • Can be 2/2 gastroenteritis or protracted diarrhea with SB villous atrophy
57
Q

Protein digestion:

A
  1. Stomach – pepsin
  2. Duodenum – pepsin is inactivated
  3. Pancreatic enzymes – continues protein digestion
  4. Colon – bacteria digest some of the remaining protein → ammonia
58
Q

The amount of ammonia absorbed is decreased when:

A
  • Reduced amount of bacteria (antibiotic administration)
  • Colonic pH is low (after lactulose administration)
59
Q

Ammonia absorption may be clinically relevant during

A
  • GI bleeds (increased absorption)
  • Liver disease (lack of conversion of enteric ammonia into urea) – can contribute to development of hepatic encephalopathy
60
Q

Fat digestion:

A
  • Mouth – lingual lipase
  • Stomach – gastric lipase
  • Duodenum – pancreatic lipase → where most fat digestion occurs
  • Bile emulsifies fat globules into smaller globules to increase surface area where water-soluble lipase enzymes can act
  • Bile salts → micelles
  • Brush border: micelles transport monoglycerides and free fatty acids to be absorbed
61
Q

Where does most fat digestion occur?

A

Duodenum via pancreatic lipase

62
Q

Pancreatic insufficiency and impact on fat digestion:

A

fat is maldigested → patients have fatty, bulky, clay-colored stools

63
Q

The absorptive area of the small intestine is approximately the same area as

A

a tennis court

64
Q

What substances are absorbed in the stomach in appreciable amounts?

A

alcohol and aspirin

65
Q

Na+ may be co-transported by carrier proteins with what?

A

amino acids or glucose

66
Q

What does sodium-glucose transporter 1 (SGLT1) help the body absorb?

A

Glucose and galactose

SGLT-1 simultaneously transports Na+ and glucose or galactose

67
Q

GLUT2

A

When intraluminal concentrations of glucose are high, glucose is absorbed via facilitated glucose transporter type 2 (GLUT2)

68
Q

How is fructose absorbed?

A

Fructose absorption into mucosal cells – facilitated diffusion by GLUT5

69
Q

High concentrations of Na+ in the chyme

A

increases glucose transport

70
Q

Low concentrations of Na+

A

decrease glucose absorption

71
Q

99% of protein consumed is absorbed before reaching what part of the bowel?

A

distal jejunum

72
Q

What is recommended as a serum cholesterol-lowering intervention and why?

A

Nonabsorbable soy-based sterols reduce cholesterol absorption

73
Q

How are fat-soluble vitamins absorbed?

A

Fat soluble vitamins are transported to the brush border within micelles (just like fatty acids)

74
Q

How are water soluble vitamins absorbed?

A

Water soluble vitamins often require Na+ cotransporters for absorption

75
Q

Folate is absorbed via

A

a proton-coupled folate transporter

76
Q

Loss of parietal cells (gastrectomy, chronic gastritis) or loss of distal ileum may lead to what sort of deficiency?

A

B12 deficiency

77
Q

What is primarily responsible for water absorption?

A

Small bowel and colon

78
Q

Na+ facilitates absorption of

A

glucose, some amino acids, and bile acids

Which is why NaCl and glucose are in oral rehydration solutions

79
Q

Protein facilitates the absorption of what?

A

calcium and magnesium

80
Q

Why does the passage of feces continue during bowel rest?

A

because fecal contents include material other than food residue

81
Q

MCTs

A

Water soluble
Hydrolyzed and pass through enterocytes directly into portal circulation

82
Q

SCFAs

A

Produced in the colon by the action of bacteria on fermentable dietary fiber

83
Q

Types of SCFAs formed:

A

acetate, propionate, and butyrate

84
Q

Effects of SCFAs

A
  • Increased sodium and water absorption
  • Trophic effects on mucosal cells of the colon
  • Inhibition of cholesterol synthesis in the liver
  • Improvement of colonic and splanchnic circulation
  • Enhancement of immunity through stimulation of the production of macrophages, T helper lymphocytes, neutrophils, and antibodies
  • Acidification of colonic pH → lower solubility of bile acids and their conversion to cytotoxic bile acids; inhibits growth of pathogenic bacteria
85
Q

What happens to the villi in low flow states (ex: circulatory collapse)?

A

Oxygen deprivation in the tips of the villi → ischemic death of villi → decreased absorptive capacity

86
Q

Mucosal atrophy occurs during

A
  • starvation
  • stress
  • PN
  • bowel rest
87
Q

the microvilli shorten

A

After 1 week of a protein deficient diet

88
Q

Glutamine is a

A

principal metabolic fuel for intestinal cells
* Its absence may contribute to mucosal atrophy that accompanies bowel rest

89
Q

Trickle feeds (10-20 ml/hr) can prevent mucosal atrophy in which patient patients?

A

low- to moderate-risk patients

  • It will not achieve the desired EN clinical outcomes in high-risk patients