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PHYSL 214 > GI Phys > Flashcards

GI Phys Flashcards

1
Q

the GI tract is (mobile/motile) to move and mix contents for digestion and absorption

A

motile

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2
Q

digestion

A

breaking down food/high-molecular weight substances into small molecules

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3
Q

absorption

A

transport of digestive products across intestinal epithelium

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4
Q

secretion

A

release of substances into lumen of GI tract to facilitate digestion/absorption/motility

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5
Q

functions of GI tract are interdependent to optimize _______

A

absorption

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6
Q

functional segmentation

A

continuous tube is separated into segments with unique functions

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7
Q

accessory organs examples (4)

A

salivary glands, liver, pancreas, gallbladder

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8
Q

accessory organs functions

A

secrete substances into GI tract to facilitate digestion/absorption (anatomically distinct)

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9
Q

9 layers of intestinal wall (cross-section)

A

epithelium, basement memb., lamina propria, muscularis mucosae, submucosa, circular muscle, myenteric plexus, longitudinal muscle, mesothelium

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10
Q

epithelium function

A

cell barrier nutrients transverse to be absorbed

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11
Q

2 circulatory structures that transport substances between tract and rest of body

A

capillaries and lymphatics

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12
Q

circular/longitudinal muscle function

A

allow motile contractions

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13
Q

myenteric plexus function

A

nerve supply controlling motility/secretion

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14
Q

endocrine cells function

A

secrete hormones into blood for digestion/appetite

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15
Q

exocrine/acinar cells function

A

secrete digestive substances/enzymes into gut lumen

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16
Q

mucous cells function

A

form ducts to connect lumen of GI tract to accessory organs

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17
Q

sphincters form/function

A

rings of muscle that constrict GI tube; regulate flow, prevent backflow

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18
Q

6 sphincters of GI tract

A
  1. upper esophageal (pharynx/eso.)
  2. lower esophageal (eso./stomach)
  3. pyloric (stomach/ sm. intes.)
  4. ileocecal (sm. intes./lg. intes.)
  5. internal anal (rectum/anus)
  6. external anal (rectum anus)
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19
Q

3 mouth functions

A

mechanical food breakdown, preparation for swallowing and onset of digestion

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20
Q

mouth: mastication definition

A

chewing (teeth/facial muscles)

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21
Q

mouth: prep. for swallowing

A

moistening bolus with saliva

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22
Q

mouth: onset of digestion

A

enzymatic breakdown via salivary amylase

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23
Q

swallowing reflex controlled by ___

A

ANS

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24
Q

swallowing: oral phase

A

voluntary collection of food bolus into pharynx by tongue

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25
Q

swallowing: pharyngeal phase

A

involuntary contractions of pharyngeal muscles, pushes bolus into esophagus

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26
Q

swallowing: esophageal phase

A

peristaltic wave moves bolus down esophagus (~4cm/s)

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27
Q

swallowing: additional reflex functions (2)

A

glottis closure and respiration inhibition

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28
Q

4 step process of swallowing

A
  1. tongue moves bolus to back of mouth, tiggers reflex (oral phase)
  2. soft palate elevates to prevent food from entering nasal passage (pharyngeal phase)
  3. epiglottis covers glottis, preventing bolus entry into trachea, upper eso. sphincter relaxes (pharyngeal phase)
  4. food descends eso. (eso. phase)
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29
Q

3 stomach funcitons

A

storage, continued digestion, regulate emptying into sm. intes.

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30
Q

2 sections of stomach

A

fundus (top) and antrum (mixing)

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31
Q

lower eso. sphincter function

A

control food entry to stomach and prevent reflux

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32
Q

stomach: mechanical digestion form

A

peristaltic waves vie rugae (folded surfaces)

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33
Q

stomach: chemical secretions (2)

A

HCl, pepsin

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34
Q

stomach: HCl functions (2)

A

acidity denatures proteins (more soluble) and cleaves pepsinogen to pepsin

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35
Q

pepsin

A

enzyme that breaks down proteins

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36
Q

chyme

A

ingested food that leaves stomach

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37
Q

3 sections of sm. intes.

A

duodenum (20cm), jejenum (2.5m), iluem (3m)

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38
Q

sm. intes. function

A

primary site of digestion

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39
Q

sm. intes. maximizes food ________

A

absorption

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40
Q

______ enzymes aid digestion in sm. intes.

A

hydrolytic

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41
Q

sm. intes. form to incr SA (4: biggest to smallest)

A

tube>circular folds>villi>microvilli (increases SA - 600 fold)

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42
Q

brush border is composed of

A

microvilli

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43
Q

incr. SA allows for…

A

incr. contact for digestrion/absorption

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44
Q

lg. intes. function

A

store and concentrate undigested material

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45
Q

lg. intes. form (7)

A

cecum, appendix, asc. colon, transverse colon, desc. colon, sigmoid colon, rectum

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46
Q

cecum form/function

A

first part of lg. intes.; small in humans, cellulose digestion in herbivores

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47
Q

appendix function

A

reserve for healthy gut bacteria (restore microflora after diarrhea)

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48
Q

asc., transverse, desc., sigmoid colon functions

A

absorption of ions and water; bacterial metabolism

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49
Q

rectum function

A

holds feces before defecation

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50
Q

salivary glands: 3 types

A

sublingual (under tongue), submandibular (under jaw), parotid (beside ear)

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51
Q

salivary glands: general form

A

empty into oral cavity

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52
Q

salivary glands: function

A

secrete water and mucus to moisten and lubricate bolus; amylase to digest large carbs.

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53
Q

liver and gallbladder: form

A

empty into sm. intes. via bile duct

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54
Q

liver: secretions and functions (4)

A

bile salts digest fats, bicarbonate neutralizes acidic chyme, org. waste products and trace metals for elimination

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55
Q

gallbladder: 3 functions

A

stores, concentrates (absorbs H2O and NaCl) and releases bile

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56
Q

exocrine pancreas: form

A

(digestive system) acinar cells secrete enzymes into sm. intes. via pancreatic duct

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57
Q

endocrine pancreas: form

A

(endocrine system) islet cells of Langerhans secrete hormones into blood (ex: insulin)

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58
Q

pancreas: secretions and functions (4)

A

bicarbonate neutralizes chyme, pancreatic amylase digests carbs., trypsinogen+chymotrypsin digest proteins, pancreatic lipase digests fats

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59
Q

peristalsis/peristaltic wave

A

rings of contraction that pass along the length of the GI tract, force lumenal contents forwards

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60
Q

segmentation

A

constriction of GI tract in situ to mix contents (no net movement, ie. back and forth)

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61
Q

peristaltic reflex triggered by…

A

lumenal contents stretching intestinal wall, causing contraction behind and relaxation in front of bolus

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62
Q

peristaltic reflex independent of…

A

external innervation but modulated by ANS input

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63
Q

peristaltic reflex dependent on…

A

ENS activity

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64
Q

peristaltic response steps (3)

A
  1. local stretch response releases serotonin (activates sensory neurons that activate myenteric plexus)
  2. “upstream” neurons activated and release factors for smooth muscle contraction
  3. “downstream” neurons activated and release factors for smooth muscle relaxation
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65
Q

2 factors that cause smooth muscle contraction in peristalsis

A

substance P and acetylcholine

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66
Q

2 factors that cause smooth muscle relaxation in peristalsis

A

NO and vasoactive intestinal polypeptide

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67
Q

segmentation primarily occurs in the…

A

small intestine

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68
Q

segmentation response steps (3)

A
  1. initial contractions separate contents into pockets
  2. next contractions separate pockets centrally
  3. rhythmic contractions continue to subdivide pockets
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69
Q

BER stands for

A

basic electrical rhythm

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70
Q

BER form and function

A

pacemaker cells (interstitial cells of Cajal); rhythmic oscillations in Vmemb. of smooth muscle cells causes contractions for segmentation

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71
Q

2 factors affecting BER rate

A
  1. acetylcholine: INCR activity and contraction

2. epinephrine: DECR activity and contraction

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72
Q

rate of BER in stomach, duodenum, ileum, cecum and sigmoid colon respectively (#/min)

A

4/min, 12/min (fastest), 8/min, 2/min (slowest), 6/min

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73
Q

MMC occurs after…

A

segmentation and food has been absorbed

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74
Q

MMC

A

migrating myoelectric complex

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75
Q

MMC function

A

move undigested contents in sm. intes. to lg. intes.

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76
Q

what is the MMC?

A

final sweeping wave of contractions from stomach to sm. intes. in 2ft long sections

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77
Q

MMC duration

A

~2 hours

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78
Q

3 phases of MMC

A
  1. quiescent period (during digestion and absorption)
  2. irregular elec./mech. activity
  3. regular elec./mech. activity
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79
Q

MMC is inhibited by… and why?

A

ingestion of a meal; want food to stay in sm. intes. for digestion and absorption

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80
Q

hormone that controls MMC

A

motilin (in plasma)

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81
Q

motilin secretion is inhibited by…

A

ingestion

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82
Q

LES activity

A

tonically active, relaxes to allow food entrance to stomach

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83
Q

why is the LES tonically active?

A

prevent stomach reflux into eso.

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84
Q

3 components of LES and definitions

A
  1. internal sphincter: thickening of eso. smooth muscle
  2. external sphincter: crural portion of diaphragm surrounds eso.
  3. clasp/sling fibers: stomach wall muscles
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85
Q

LES

A

lower eso. sphincter

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86
Q

VIP

A

vasoactive intestinal polypeptide

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87
Q

3 factors that affect LES contraction/relaxation

A

ACh: contracts

NO and VIP: relaxes

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88
Q

receptive relaxation

A

stomach relaxation to allow incr V without incr P (compliance)

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89
Q

overfilling of stomach effects

A

belching or vomiting

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90
Q

gastric peristalsis function

A

mixes stomach contents and pushes them through pyloric sphincter

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91
Q

gastric peristalsis generated by…rate?

A

basic electrical rhythm (F is extrinsically controlled); ~3/min

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92
Q

gastric peristalsis process

A

starts at top of stomach and incr in size as it moves down, forces pyloric sphincter closed with some liquid chyme forced through

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93
Q

4 extrinsic factors controlling gastric emptying

A

stomach/intestinal contents, acidity, distension, hypertonicity

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94
Q

stomach contents effect on gastric emptying

A

meals rich in protein or fat delay gastric emptying

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95
Q

acidity effect on gastric emptying

A

acidity inhibits gastric emptying (feedback loop w/ duodenum)

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96
Q

distension effect on gastric emptying

A

stomach distension incr peristaltic contractions, duodenum distension inhibits gastric emptying

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97
Q

chyme tonicity in intes. effect on gastric emptying

A

isotonic duodenal contents incr gastric emptying; hypertonic decr gastric emptying

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98
Q

belching/aerophagia

A

physiological venting of gastric air

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99
Q

belching/aerophagia cause

A

air swallowed during drinking or eating

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100
Q

belching/aerophagia process

A

air in stomach incr gastric V, reflex response relaxes LES allowing air to escape

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101
Q

vomiting/emesis

A

involuntary, forceful expulsion of stomach contents out of mouth

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102
Q

vomiting/emesis regulators (2)

A

CNS: nucleus tractus solitarius and brain stem vomiting center

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103
Q

vomiting/emesis process (4)

A
  1. salivation and nausea
  2. reverse peristalsis starts from intestine and sweeps upwards
  3. ab. wall muscles contract (incr P)
  4. sphincters and eso. relax
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104
Q

5 vomiting/emesis triggers

A

digestive, sensory, emetics, social cues, miscellaneous

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105
Q

digestive vomiting/emesis triggers ex

A

gastroenteritis, bowel obstruction, food allergy

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106
Q

sensory vomiting/emesis triggers ex

A

motion sickness, viral infection, morning sickness, drug rxn

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107
Q

emetics

A

medically administered drugs to prevent poisoning by causing vomiting/emesis

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108
Q

social cues vomiting/emesis trigger ex

A

emotional distress

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109
Q

miscellaneous vomiting/emesis triggers ex

A

nauseating sights/smells, anxiety

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110
Q

different vomiting/emesis triggers act through _____ neural pathways

A

different

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111
Q

1 minor and 3 major forms of sm. intes. motility

A

minor: peristalsis
major: segmentation (during digestion), MMC, tonic contractions

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112
Q

sm. intes. segmentation controlled by

A

BER (basic electric rhythm)

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113
Q

tonic contractions are… and why?

A

prolonged contractions that can isolate segments of sm. intes.; incr t for absorption

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114
Q

sm to lg. intes. valve name and function

A

ileocecal valve; one-way to prevent backflow (incr colon P closes it, incr ileal P opens it)

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115
Q

gastroileal reflex

A

opening of ileocecal valve when food leaves stomach

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116
Q

lg. intes. motility (4)

A

segmentation, peristalsis, mass action contractions, defecation

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117
Q

mass action contractions and rate

A

simultaneous contractions of large areas of colon; 10/day

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118
Q

mass action contractions function

A

move material through colon and to rectum

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119
Q

defecation reflex caused by…

A

incr rectal P caused by mass action contractions (desire to defecate)

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120
Q

2 anal sphincter differences

A

internal: involuntary, smooth muscle
external: voluntary, skeletal muscle

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121
Q

defecation process

A

incr rectal P causes internal anal sphincter to relax and external to contract

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122
Q

> 55mm Hg P in rectum causes what to happen?

A

external anal sphincter reflexively relaxes and feces is released

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123
Q

voluntary contraction of external anal sphincter causes…

A

feces to move back into sigmoid colon due to prolonged distention, urge to defecate subsides until next mass action contraction

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124
Q

voluntary contraction of ab. muscles and relaxation of puborectalis causes..

A

descent of pelvic floor and opening of anorectal angle to facilitate defecation

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125
Q

best position to defecate and why?

A

squatting (not sitting); decr P and incidence of hemorrhoids and diverticular disease

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126
Q

transit time through GI tract avg for adults and children

A

adults: >50 hours
children: ~33 hours

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127
Q

transit time through GI tract variables

A

type of food and health status (diarrhea and constipation)

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128
Q

transit time through stomach, sm. intes. and colon (hours)

A

stomach: 4-5 hours
sm. intes. 2.5-3 hours
colon: 30-40 hours
(~2 days total)

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129
Q

4 factors of luminal comp. that affect GI responses

A

V of luminal contents, osmolarity, acidity, nutrient comp.

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130
Q

V of luminal contents: receptor type and effector

A

(distension) mechanoreceptors, smooth muscle cells

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131
Q

osmolarity: receptor type and effector

A

([solute]) osmoreceptors, exocrine glands

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132
Q

acidity: receptor type and effector

A

(pH) chemoreceptors, exocrine glands

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133
Q

nutrient comp.: receptor type and effector

A

(macromolecule type) chemoreceptors, exocrine glands

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134
Q

2 plexuses of ENS

A

submucosal and myenteric plexuses

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135
Q

difference btwn short and long reflexes

A

short reflexes: signal within ENS

long reflexes: signal integrated with CNS

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136
Q

enteroendocrine cells: form

A

cell in intestinal wall: apical side faces lumen, basolateral side faces interstitial space

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137
Q

enteroendocrine cells: function

A

receive stimuli from intestinal lumen and secrete hormones into interstitial space->bloodstream

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138
Q

4 GI hormones

A

gastrin, cholecystokinin, secretin, glucose-dependent peptide

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139
Q

CCK stands for…

A

cholecystokinin

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140
Q

GIP stands for…

A

glucose-dependent insulinotropic peptide

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141
Q

gastrin: site of production

A

stomach

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142
Q

gastrin: production trigger

A

aa/peptides

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143
Q

gastrin: response in stomach

A

stimulates HCl secretion and motility

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144
Q

CCK: site of production

A

sm. intes.

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145
Q

CCK: production trigger

A

aa and fat

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146
Q

CCK: response in stomach

A

inhibits acid secretion and motility

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147
Q

CCK: response in pancreas

A

stimulates enzymes secretion

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148
Q

CCK: gallbladder response

A

stimulates contraction of gallbladder and relaxation of sphincter of Oddi (to secrete bile)

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149
Q

secretin: site of production

A

sm. intes.

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150
Q

secretin: production trigger

A

acidity

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151
Q

secretin: response in stomach

A

inhibits HCl secretion and motility

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152
Q

secretin: response in pancreas and liver

A

stimulates release of HCO3

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153
Q

GIP: site of production

A

sm. intes.

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154
Q

GIP: production trigger

A

glucose and fat

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155
Q

GIP: response in pancreas

A

stimulates insulin secretion

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156
Q

3 phases of GI regulation

A

cephalic, gastric, intestinal

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157
Q

cephalic phase

A

sight, smell, taste of food stimulates brain

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158
Q

gastric phase

A

distension, acidity, aa/peptides stimulates stomach

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159
Q

intestinal phase

A

distension, acidity, osmolarity, digestive products stimulates intestine

160
Q

approx. daily volume of secretions into GI tract

A

~7 L (vs 1.2 L daily fluid intake)

161
Q

approx. daily volume of fluid lost in feces

A

~0.1 L (majority of fluid is reabsorbed)

162
Q

major producers of secretions into GI tract

A

accessory glands (salivary glands, liver, gallbladder, exocrine pancreas)

163
Q

approx. daily V of salivary secretions

A

1.5 L

164
Q

5 saliva components

A

water (98%), electrolytes, mucus, enzymes, immune modulators

165
Q

water, electrolytes and mucus function in saliva

A

lubrication to protect oral cavity and ease of swallowing

166
Q

immune modulators function in saliva

A

antibacterial antibodies, WBCs, etc. to kill pathogens

167
Q

salivary secretion regulation during the ______ phase

A

cephalic

168
Q

salivary secretions regulated by ___ nervous system

A

autonomic (para/symp)

169
Q

para vs symp regulation of salivary secretion viscosity

A

symp: thicker
para: watery

170
Q

para vs symp regulation of salivary secretion viscosity function

A

symp: thicker = respiration
para: watery = digestion

171
Q

para vs symp regulation of salivary secretion primary NT

A

symp: NE
para: ACh

172
Q

symp regulation of salivary secretion ex (anxiety)

A

anxiety = incr symp. activity = decr salivation/thickening = dry mouth

173
Q

para regulation of salivary secretion ex

A

appetizing food = incr para = incr salivation

174
Q

approx. daily V of gastric secretions

A

2 L

175
Q

4 components of gastric secretions

A

Mucus, HCL, enzymes, hormones

176
Q

gastric mucus function

A

lubricates and protects stomach lining

177
Q

gastric HCl function (3)

A

solubilizes food (proteins), kills ingested microbes, cleaves pepsinogen to pepsin

178
Q

gastric enzyme ex and function

A

pepsin (proteolytic enzyme-cleaves proteins)

179
Q

gastric hormones function

A

regulate other gastric secretions (secreted into blood not stomach)

180
Q

gastric 2 types of mucus-producing cells

A

surface and neck mucus cells

181
Q

gastric HCl-producing cells

A

parietal cells

182
Q

gastric histamine-producing cells

A

enterochromaffin-like (ECL) cells

183
Q

gastric pepsinogen-producing cells

A

chief cells

184
Q

5 cells in gastric gland from inside->out

A

chief, ECL, parietal, mucous neck, surface mucous

185
Q

HCl production is mediated by which 2 phases

A

cephalic and gastric

186
Q

3 compounds that stimulate HCl/H+ production from parietal cells

A

gastrin, histamine, ACh

187
Q

compound that inhibits HCl/H+ production from parietal cells

A

somatostatin

188
Q

how do compounds that stimulate/inhibit HCl/H+ production from parietal cells work?

A

via 2nd messengers, binding of ligand stimulates exocytosis of vesicles with H+/K+-ATPase pumps onto cell pmemb.

189
Q

what are 2 ways that HCl/H+ production from parietal cells is stimulated?

A

G-cells in intes. epi produce gastrin (after high protein meal), enters circulation and stimulates parietal cells to produce HCl directly or through ECL cells by incr histamine production

190
Q

what did the experiments on Alexis St. Martin by William Beaumont show?

A

the stomach could digest food without the mouth’s chewing

191
Q

approx. daily V of pancreatic secretions

A

1.5 L

192
Q

2 components of pancreatic juice

A

bicarbonate and enzymes

193
Q

pancreatic bicarbonate function

A

neutralizes chyme

194
Q

pancreatic enzymes function

A

breakdown macromolecules

195
Q

pancreatic duct cells secrete

A

bicarbonate

196
Q

main pancreatic duct: form

A

drains pancreatic glands and merges with common bile ducts from gallbladder and liver before entering sm. intestine

197
Q

pancreatic secretions are controlled in which phase

A

intestinal (with cephalic and gastric inputs)

198
Q

if the chyme is acidic, what will the sm. intes., pancreas and liver secrete? (+feedback loop)

A

sm. intes. produces secretin which incr pancreas+liver bicarbonate production, sm. intes. is neutralized which feedback inhibits sm. intes. secretin production

199
Q

if there is lots of intes. fa and aa, what will the sm. intes. and pancreas secrete? (+feedback loop)

A

sm. intes. produces CCK which incr pancreas enzyme production, sm. intes. has incr digestion which feedback inhibits sm. intes. CCK production

200
Q

how do hormones travel/signal between the sm. intes. and pancreas?

A

blood (in plasma)

201
Q

approx. daily V of bile from the liver

A

0.5 L

202
Q

bile is produced by the…

A

liver

203
Q

bile is stored in the…

A

gallbladder

204
Q

7 components of bile

A

water (97%), bile salts, bile pigments, cholesterol, inorganic salts, fa, and phosphatidylcholine

205
Q

bile salts function in bile

A

solubilize water-insoluble fats (cholesterol)

206
Q

bilirubin function in bile

A

product of Hb breakdown (excreted)

207
Q

fat form and function in bile

A

phospholipids (cholesterol and lecithin), aid fat digestion

208
Q

how does bile accumulate in the gallbladder?

A

continuously produced by liver in dilute form, some diverted into gallbladder or builds up when sphincter of Oddi is closed (cant flow into duodenum)

209
Q

what is absorbed from bile in the gallbladder?

A

water and salts (NaCl), making it more concentrated

210
Q

in response to CCK the gallbladder…

A

contracts and sphincter of Oddi relaxes, bile enters duodenum

211
Q

during what phase is bile secretion regulated?

A

intestinal

212
Q

how is bile secretion regulated in duodenum and gallbladder?

A

if duodenum has high [fa], incr CCK secretion, gallbladder secretes bile (into common bile duct) and sphincter of Oddi relaxes (flows into duodenum)

213
Q

approx. daily V of intestinal secretions

A

1.5 L

214
Q

3 components of intestinal secretions

A

water/electrolytes, mucus, and enzymes

215
Q

water/electrolytes function in intes. secretions

A

maintains fluidity of intes. contents

216
Q

mucus function in intes. secretions

A

lubrication and protection of epithelium lining

217
Q

enzymes function in intes. secretions

A

aids digestion

218
Q

what drives water secretion in intes.?

A

osmosis

219
Q

what are intestinal crypts?

A

invaginations of intes. wall surrounding base of villi

220
Q

diff btwn function of crypts vs villi?

A

crypts: secretory function
villi: absorptive function

221
Q

what do epi. cells in crypts secrete?

A

ions: Na, Cl, HCO3, water follows by osmosis

222
Q

how does chyme leaving stomach affect osmolarity of sm. intes.?

A

high [solute] creates hypertonic enviro and pulls water from plasma by osmosis

223
Q

how much of GI secretions are absorbed?

A

6.7 L (most)

224
Q

which 3 types of macronutrients are required in the diet?

A

fats, carbs, protein

225
Q

what is the cal/g ratio for carbs?

A

4 cal/g

226
Q

what is a non-digestible carb?

A

dietary fiber

227
Q

what does hydrolyzed lactose form?

A

glucose + galactose

228
Q

what does hydrolyzed maltose form?

A

2 glucose

229
Q

what does hydrolyzed sucrose form?

A

glucose + fructose

230
Q

why can’t cellulose be digested?

A

alternating orientation of glucose residues, linked by H-bonds, makes it harder for catalytic enzymes to cleave them

231
Q

what is the cal/g ratio for dietary fats?

A

9 cal/g (most)

232
Q

what is the most abundant type of dietary fat?

A

triglyceride (~90%)

233
Q

what is the structure of triglycerides?

A

glycerol + 3 fa

234
Q

what 3 forms of triglyceride fatty acids are there?

A

saturated, mono-unsaturated, poly-unsaturated

235
Q

what is the cal/g ratio for proteins?

A

4 cal/g

236
Q

what is a major feature of fats, carbs and proteins?

A

major source of energy

237
Q

what differentiates proteins from fats and carbs?

A

more considered a building block than an energy source

238
Q

what are supramolecular protein assemblies? and 3 ex?

A

multiple different proteins associated to form biological machines; protein complexes, myofilaments, collagen fibrils

239
Q

what are 3 different types of micronutrients?

A

fat-soluble vitamins, water-soluble vitamins and trace elements

240
Q

what are 3 ex of fat-soluble vitamins?

A

A, E, D

241
Q

what are 2 ex of water-soluble vitamins?

A

B complex, C

242
Q

what are 4 ex of trace elements?

A

iron, iodine, zinc, calcium

243
Q

what specific type of enzyme is amylase?

A

alpha(1,4) endoglucosidase (cleaves glycosidic bonds btwn 4C and 1C in polysacc. to form oligo/disacc.)

244
Q

where and what are brush border enzymes?

A

sm. intes.; enzymes on brush border of intes. epi. that are specific to different disacc.

245
Q

what are the brush border enzymes for maltose, sucrose and lactose?

A

maltase, sucrase, lactase

246
Q

what is lactaid? why is it used?

A

lactase enzyme; for lactose intolerance (deficiency of lactase, can’t breakdown lactose)

247
Q

how are glucose and galactose absorbed in intes. epi cell? (2)

A

secondary active transport, SGLT-1

248
Q

what is SGLT-1?

A

sodium-glucose cotransporter, imports 2 Na down conc grad. and 1 glucose/galactose up conc. grad. (2ndary active transport)

249
Q

what is GLUT2

A

glucose transporter, exports glucose/galactose down conc. grad. (facilitated diffusion)

250
Q

how and why are Na ions removed from intes. epi cell?

A

Na/K ATPase; to maintain low [Na] conc. inside cell for SGLT-1

251
Q

what 2 transporters are on the apical side of the intes. epi. cell?

A

SGLT-1 and GLUT5

252
Q

what 2 transporters are on the basolateral side of the membrane?

A

GLUT2 and Na/K ATPase

253
Q

how is fructose absorbed? (2)

A

facilitated diffusion, GLUT5

254
Q

what proteins transport fructose in vs out of the intes. epi. cell?

A

GLUT5 and GLUT2

255
Q

what occurs during a high-sugar meal in an intes. epi. cell?

A

sugar gradients are saturated so GLUT2 is translocated from basolateral to apical side of cell to aid diffusion of sugar into cell (max. absorption)

256
Q

what is the general summary of carb. digestion and absorption?

A

pancreatic amylase cleaves polysacc. to oligo/disacc. in intes. lumen, brush border enzymes cleave to monosacc. which are transported across intes. epi. cell

257
Q

what are 3 ex of dietary fibers?

A

cellulose (plant cell walls), lignin (plant cell walls), chitin (cell walls of fungi & insect/crustacean exoskeletons)

258
Q

what are 4 physl. effects of dietary fibers?

A
  1. delays gastric emptying and incr fullness
  2. decr absorption in sm. intes.
  3. fiber fermentation in lg. intes.
  4. fecal bulking
259
Q

what are 3 effects of trapping, interfering, and inhibiting by dietary fibers (decr sm. intes. absorption)?

A

delays carb. absorption (better glucose control), impairs cholesterol absorption, trapping trace elements or toxic compounds

260
Q

what is fiber fermentation?

A

gut microbiota can ferment undigested fiber to produce short-chain fa (energy source)

261
Q

what is fecal bulking?

A

mass of undigested fiber can retain water and incr bacterial mass secondary to fiber fermentation

262
Q

g of fat in avg. diet and % of cal. intake

A

65-95g; ~35%

263
Q

what % of ingested fat is absorbed?

A

95%

264
Q

what are triglycerides broken down into?

A

free fatty acids

265
Q

what is a unique aspect of fat digestion?

A

lipids form large globules of fat in water and must be emulsified

266
Q

emulsification requires what 2 things

A
  1. mechanical digestion

2. emulsifying agents

267
Q

where are emulsifying agents contained? and what are they made of

A

bile; phospholipids and bile salts (amphipathic molecules)

268
Q

what is lipolysis?

A

process of fat breakdown

269
Q

what are the products of lipolysis?

A

monoglycerides and free fatty acids

270
Q

what is lipolysis catalyzed by?

A

pancreatic lipases

271
Q

why is colipase needed and what does it do

A

pancreatic lipase is water-soluble so colipase is required to hold pancreatic lipase to lipid droplet surface

272
Q

what do the products of lipolysis form at high conc.?

A

micelles (combined with bile salts)

273
Q

micelle formation and breakdown existing in an equil. allows for what?

A

small fraction of fat-digestion products to be dissolved in solution and absorbed

274
Q

how do solubilized fa cross the intes. epi. cell memb? (2)

A

diffusion; “flip-flop”

275
Q

what are chylomicrons?

A

repackaged triglycerides coated in apolipoproteins in intest. epi. for secretion (via exocytosis)

276
Q

why are chylomicrons formed?

A

easier to transport throughout body vs free fa and monoglycerides

277
Q

what is a summary of fat digestion and absorption? (4)

A

emulsification, lipolysis, diffusion, chylomicron formation and secretion

278
Q

required vs avg. g of protein ingested

A

40-50, 60-90

279
Q

where else does the intestine receive proteins other than from ingestion?

A

secreted into it from mucus, enzymes and degraded epi. cells

280
Q

what % of protein is broken down into aa and absorbed?

A

95% (regardless of source)

281
Q

what enzyme mediates protein digestion?

A

proteolytic enzymes (proteases)

282
Q

what are 2 categories of proteases and the difference?

A

endopeptidases: cleave proteins at interior peptide bonds
exopeptidases: cleave proteins at n/c-termini

283
Q

what must occur with proteases for them to work? why?

A

activation by other proteins in lumen; very powerful and cant always be active

284
Q

what are the 2 types of exopeptidases?

A

aminopeptidases: cleave at n-term.
carboxypeptidases: cleave at c-term.

285
Q

what are 3 examples of endopeptidases?

A

trypsin, chymotrypsin, elastase

286
Q

where does protein digestion begin?

A

stomach

287
Q

what 2 ways does the stomach initiate protein digestion?

A

acidic enviro denatures proteins, secreted pepsin cleaves large polypeptides (protease)

288
Q

how is pepsin activated?

A

gastric acid cleaves pepsinogen to pepsin (stops in duodenum-alkali enviro)

289
Q

what 2 proteases continue protein digestion in the sm. intes.?

A

pancreatic and intestinal brush border enzymes

290
Q

what 2 molecules activate pancreatic enzymes?

A

enterokinase and trypsin

291
Q

how does enterokinase work?

A

bound to intes. epi. and cleaves trypsinogen to trypsin

292
Q

what can trypsin do? (2)

A

activate more trypsinogen (feedforward) and other pancreatic enzymes

293
Q

what are 3 types of intes. brush border enzymes?

A

aminopeptidases, carboxypeptidases and endopeptidases (have specific types)

294
Q

what do brush border enzymes cleave proteins into?

A

aa, di and tripeptides

295
Q

how are di and tri peptides in intes. epi. cells broken down?

A

intracellular peptidases break down to aa

296
Q

what 3 locations in the intes. does protein digestion occur? (cross-section)

A

lumen, brush border, epi. cells

297
Q

what transport protein aids di and tripeptide absorption across the intes. epi?

A

PepT1 (peptide transporter 1)

298
Q

how does PepT1 work?

A

secondary active transport of small peptides across intes. epi. with H+ (down grad.)

299
Q

how do aa exit the intes. epi cells into the interstitial space?

A

facilitated diffusion (aa transporters)

300
Q

what maintains the proton grad. for small peptide uptake in the intes. epi.?

A

NHE (apical Na/H exchanger - H out/Na in, both up grad.)

301
Q

what maintains the Na grad. for small peptide uptake in the intes. epi.?

A

Na/K ATPase (maintain low intracell. [Na]), K exits via facilitated diffusion

302
Q

what do transporters that facilitate aa uptake into intes. epi cells rely on?

A

secondary active transport with Na ions (down grad)

303
Q

what is the difference btwn small peptide vs aa uptake into intes. epi. cell?

A

small peptide: secondary active transport coupled to H ions

aa: secondary active transport coupled to Na ions

304
Q

what is a general summary of protein breakdown/absorption? (5)

A

proteins breakdown to small peptides or aa by pancreatic proteases/peptidases, small peptides broken down to aa by brush border enzymes, aa and small peptides transported into intes. epi. cells, small peptides broken down to aa by peptidases, aa exit via facilitated diffusion

305
Q

what is vit C also known as?

A

ascorbic acid

306
Q

where are majority of water-soluble vit absorbed?

A

first part of small intes

307
Q

how are water-soluble vit absorbed?

A

coupled to sodium cotransporters (except B12 and folate)

308
Q

how does vit B12 absorption occur?

A

requires binding to intrinsic factor in ileum

309
Q

how does B9/folate absorption occur?

A

proton-coupled folate transporter

310
Q

how are fat-soluble vit digested?

A

(consumed as esters) hydrolyzed in gut lumen

311
Q

how are fat-soluble vit absorbed?

A

uptake via specific transport proteins, re-esterified and packaged into chylomicrons in intes. epi.

312
Q

where is iron found in body? (3)

A

majority in Hb, some bound to ferritin, least bound to Mb

313
Q

why is iron absorption tightly regulated?

A

so amount taken up = amount lost

314
Q

What form of iron is found in diet and what form is absorbed?

A

Ferric/3+; ferrous/2+

315
Q

What reduces ferric to ferrous iron in intestine brush border?

A

Ferric reductase

316
Q

What takes up ferrous iron into enterocytes?

A

DMT1 (divalent metal transporter 1)

317
Q

What occurs to ferrous iron once in enterocytes?

A

Fe2+ is stored and bound to ferritin, remainder ferrous iron transported into circulation

318
Q

What exports remaining Fe2+ out of enterocytes?

A

Basolateral transporter ferroportin 1 (FP)

319
Q

What occurs to ferrous iron once in circulation?

A

Converted to ferric (Fe3+) and binds to transferrin (transport protein)

320
Q

What’s the difference between carb, fat and protein absorption in intes. epi?

A

Carb: secondary active transport->facilitated diffusion
Protein: secondary active transport->facilitated diffusion
Fat: diffusion->exocytosis

321
Q

How many in 10 adults were considered obese in 2016?

A

4/10

322
Q

What occurs if fat absorption is blocked?

A

Diarrhea (fatty=steatorrhea)

323
Q

where is the liver located?

A

under diaphragm and abdominal cavity

324
Q

what do absorptive segments of the GI tract drain into?

A

hepatic portal vein

325
Q

what is the hepatic portal system?

A

hepatic portal vein drains from GI and supplies liver (substances absorbed in intes. must pass through liver before entering circulation)

326
Q

where does the liver receive blood from?

A

aorta and hepatic portal vein (drains into vena cava)

327
Q

what are the hepatic lobules?

A

regular, repeating structure of liver with central vein and 6 portal triads (hexagon)

328
Q

what is the hepatic portal triad?

A

unit of hepatic lobule with portal vein, hepatic artery and bile duct

329
Q

what is the function of the portal vein of the portal triad?

A

percolates blood btwn hepatocytes and empties into central vein (towards center)

330
Q

what is the function of the hepatic artery of the portal triad?

A

oxygenates hepatocytes and drains arterial blood into central vein (towards center)

331
Q

what is the function of the bile duct of the portal triad?

A

drains bile produced by hepatocytes (towards periphery of hepatic lobule)

332
Q

what direction does bile and arterial and venous blood flow in hepatic sinusoids?

A

bile: from hepatocyte to bile duct (outwards)
arterial: artery to CV (inwards)
venous: portal vein to CV (inwards)

333
Q

what is the functional anatomy of hepatic lobules (how do hepatocytes receive blood)?

A

gaps btwn endothelial cells (fenestrations) allows blood to flow into space of Disse and come into contact with hepatocytes

334
Q

what are 3 ways the liver serves its role in whole-body carb metabolism?

A
  1. glycogen storage (glycogenesis, glycogenolysis)
  2. glucose synthesis (gluconeogenesis)
  3. buffers blood glucose levels (takes up glucose postprandially, secretes it as needed)
335
Q

what are 4 ways the liver serves its role in whole-body lipid metabolism?

A
  1. stores lipids as triglycerides
  2. energy production (beta-oxidation)
  3. De novo lipogenesis (lipid formation)
  4. lipoprotein secretion (TGL as VLDL)
336
Q

why is lipid storage in the liver problematic?

A

non-alcoholic fatty liver disease

337
Q

which enzymes play a role in detoxification in the liver?

A

cytochrome P450 family (CYPs)

338
Q

what is the general activity of CYPs?

A

detoxify xenobiotics and toxins through oxidation

339
Q

what is the most common rxn catalyzed by CYPs?

A

mono-oxygenase rxn (incorporation of a hydroxyl group)

340
Q

what is the general mono-oxidation rxn?

A

RH + O2 + NADPH + H+ –> ROH + H2O + NADP+

341
Q

how does mono-oxidation aid detoxyfication?

A

-OH group makes molecule more polar, water-soluble and easier to secrete

342
Q

what does CYP2E1 do?

A

turns ethanol into acetaldehyde (high alcohol consumption)

343
Q

why is it important not to drink alcohol while on medication?

A

ex: acetaminophen normally broken down by glucuronidation, but CYP2E1 (high w/ alcohol) will produce a toxic metabolite

344
Q

why must [ammonia] be tightly regulated?

A

membrane-permeable and toxic to CNS

345
Q

how is ammonia generated in the body?

A

amino acid metabolism

346
Q

what is ammonia metabolized to in a hepatocyte?

A

urea

347
Q

how is ammonia excreted from the body? % as urine and feces?

A

urea can diffuse into circulation (from liver) and be excreted; 75% urine and 25% feces

348
Q

the liver can regrow from __% of its original size

A

25

349
Q

living liver donor can donate __-__% of their liver

A

40-60%

350
Q

what is liver fibrosis?

A

scar tissue forms on liver

351
Q

what is liver cirrhosis?

A

growth of connective tissue destroys liver cells

352
Q

bile is secreted by hepatocyte into….

A

bile canaliculi (drains into bile ducts)

353
Q

what is the enterohepatic circulation? (form)

A

Circulation of gallbladder/liver secretions into duodenum via common bile duct and reabsorbed in ileum by hepatic portal vein

354
Q

what causes the yellow-green colour of bile?

A

bile pigments: bilirubin and biliverdin

355
Q

what are bilirubin and biliverdin products of?

A

Hb catabolism from RBC breakdown in liver and spleen

356
Q

what is bilirubin bound to in circulation?

A

albumin

357
Q

what is bilirubin metabolized into in hepatocytes?

A

bilirubin glucuronide

358
Q

what is the benefit of converting bilirubin to bilirubin glucuronide?

A

more water soluble (transported into bile canaliculi for secretion)

359
Q

what is jaundice?

A

yellowing of body tissues due to bilirubin accumulation

360
Q

what are the prehepatic, hepatic and posthepatic origins of jaundice?

A

pre: incr breakdown of RBCs
hepatic: liver disease (cant metabolize bilirubin)
post: obstruction of bile secretion

361
Q

what is hyperbilirubinemia?

A

high levels of bilirubin in circulation and accumulation in CNS (can cause brain damage)

362
Q

what causes neonatal jaundice?

A

breakdown of fetal Hb and delayed maturation of metabolic pathways in liver

363
Q

how is neonatal jaundice treated? why?

A

phototherapy; blue light catalyzes isomerization of trans- to cis- isomer of bilirubin w/ incr water solubility

364
Q

how does the stomach not digest itself? (3)

A

mucus-bicarbonate barrier btwn lumen and epi. cells (alkaline-neutralizes stomach acid), tight junctions btwn epi. cells (no leak of acid into ISS), epi. cell turnover (replace damaged cells)

365
Q

what does breakdown of the mucus-bicarbonate barrier in the stomach lead to?

A

erosion of the gastric epi. and ulcers

366
Q

what was believed to be the cause of ulcers? (historically vs experimental)

A

Historically: stress

Barry Marshall: infection (Helicobacter pylori)

367
Q

what % of duodenal vs gastric ulcers are caused by Helicobacter pylori?

A

duodenal: 90%
gastric: 80

368
Q

how can stomach ulcers be diagnosed? (4)

A

medical history/physical exam, test for H. pylori, endoscopy, barium meal + x-ray

369
Q

how can stomach ulcers be treated? (4)

A

antibiotics (if H. pylori +), antacid (short term), or inhibit stomach acid production w/ histamine blockers (block receptors on parietal cells) or proton pump inhibitors (inhibits H/K ATPases on parietal cells)

370
Q

what are 2 types of gallstones?

A
  1. cholesterol (85% in developed world)

2. calcium bicarbonate

371
Q

how do cholesterol stones develop?

A

[cholesterol] in bile incr until it precipitates out of solution into crystals (as micelles)

372
Q

what can cause incr biliary [cholesterol]?

A

incr hepatic secretion of cholesterol or too much ion+water absorption

373
Q

what are the effects of small vs large gallstones in the gallbladder?

A

small: easily passed from gallbladder to intes. and excreted
larger: get trapped leaving gallbladder (painful but bile secretion can occur from liver)

374
Q

what are the effects of large gallstones trapped in the common bile duct? (3)

A

bile secretion is impaired and decr digestion/absorption of fats (diarrhea) and fat-soluble vitamins

375
Q

what does backflow of bile cause? (3)

A

inhibition of its secretion, decr bilirubin excretion and obstructive jaundice

376
Q

what are the effects of large gallstones trapped in the ampulla of vater? (3)

A

blocks bile/pancreatic secretions, decr nutrient digestion/absorption and nutritional deficiency

377
Q

how can gallstones be diagnosed? (3)

A

medical history/medical exam, ultrasound, CT scan

378
Q

how can gallstones be treated? (3)

A

asymptomatic (no treatment), medication to dissolve them (ursodiol-bile salt, helps cholesterol stay dissolved), surgical removal of gallbladder (laparoscopic cholecystectomy)

379
Q

is it possible to live without the gallbladder? effect?

A

yes; harder to digest fats

380
Q

what is colitis?

A

inflammation of inner lining of colon

381
Q

what are the symptoms of colitis? (4)

A

abdominal pain, cramping, diarrhea, others depending on cause

382
Q

what are 4 causes of colitis?

A

infection, inflammatory bowel disease (Crohn’s disease or ulcerative colitis), allergic rxn (gluten), ischemia (decr blood supply)

383
Q

what bacteria causes infectious colitis?

A

clostridium difficile (C. diff)

384
Q

what is C. diff?

A

gram + spore-forming bacteria

385
Q

is C. diff a constituent of gut microbiome?

A

yes (vegetative)

386
Q

in what individuals is C. diff typically found?

A

neonates, 2-5% of adults (if normal immune response)

387
Q

what are 2 impacts of C. diff?

A

leading cause of health-care associated diarrhea and community acquired colitis

388
Q

what does “health-care associated” disease mean?

A

nosocomial infection: originated in a hospital (antibiotic exposure)

389
Q

what is the spectrum of C. diff symptoms if failure to mount immune response? (6)

A

self-limiting diarrhea, fulminant colitis, pseudomembranous colitis, toxic megacolon, bowel perforation/sepsis and multiple organ failure

390
Q

what is the life cycle of C. diff in the body?

A

spores enter through mouth, resistant to gastric acid/digestive enzymes, exposed to E source in sm. intes. (activate spores to bacteria), colonize colon and produce toxins (biofilm formation)

391
Q

what are the pros and cons of antibiotics to treat C. diff?

A

pro: effective
cons: antibiotic resistance, broad-spectrum antibiotics can cause recurrent infections (need narrow spectrum)

392
Q

what is another way to treat colitis? (not antibiotics)

A

fecal microbiota transplant (FMT)

393
Q

what is fecal microbiota transplant?

A

transplant healthy bacteria (from stool) to diseased patient (in pill)

394
Q

what are the barriers for fecal microbiota transplant? (3)

A

public acceptance, safety, standardization/identification of bacterial signatures (ensure donor is healthy)

395
Q

pancreatic acinar cell secretions (4)

A

pancreatic amylase, pancreatic lipase, chymotrypsin, and trypsinogen

396
Q

how are pentose sugars absorbed in the sm. intes?

A

diffusion (ribose)

PHYSL 214 (6 decks)

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