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Physiology > Gastrointestinal > Flashcards

Gastrointestinal Flashcards

1
Q

functions of GI tract

A

transfers digested organic nutrients, minerals and water from the external environment to the internal environment

excretion

host defense

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2
Q

digestion

A

chemical alteration of food into absorbable molecules
GI motility, pH changes, biological detergents, and enzymes

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3
Q

absorption

A

movement of digested food from the intestine into the blood or lymphatic system

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4
Q

excretion

A

non-absorbable components of food, bacteria, intestinal cells, hydrophobic molecules (drugs, cholesterol, steroids)

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5
Q

immune system

A

GIT is continuous with exterior of body = potential portal for harmful substances + microorganisms
highly developed immune system

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6
Q

components of GI tract

A

mouth
pharynx
esophagus
stomach
small intestine
large intestine

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7
Q

accessory organs

A

help breakdown food

pancreas
liver
gall bladder
salivary glands

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8
Q

GI tract

A

long muscular tube stretching from mouth to anus
similar composition from mid-esophagus to anus

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9
Q

GIT structure

A

from inside to outside

mucosa
submucosa
muscularis externa
serosa

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10
Q

mucosa

A

epithelium
lamina propria
muscularis mucosa

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11
Q

epithelial layer of mucosa

A

layer of cells that lines all body cavities and surfaces
provides selective uptake of nutrients, electrolytes, + H2O; prevents passage of harmful substances

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12
Q

epithelium is polarized

A

basolateral + apical arrangements (two different surfaces) → have different transport proteins

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13
Q

villi + crypts

A

increase surface area
villi: projections into lumen
crypts: indentations

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14
Q

stem cells in crypts

A

divide + differentiate → daughter cells migrate upwards towards villi

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15
Q

paracellular pathway

A

selective transport of nutrients across epithelium
limited by tight junction seal
only water and small ions can diffuse in between cells

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16
Q

transcellular pathway

A

selective transport of nutrients across epithelium
two step process
requires transport proteins on both apical and basolateral surfaces of cell

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17
Q

lamina propria

A

made of connective tissue, small blood vessels, nerve fibres, lymphatic vessels, and immune + inflammatory cells

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18
Q

muscularis mucosa

A

thin layer of smooth muscle
not involved in peristalsis (contraction)
movement of villi

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19
Q

submucosa

A

composed of connective tissue, blood + lymphatic vessels
plexus of nerve cell bodies

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20
Q

submucosal plexus

A

relay information to and from mucosa

intrinsic neural regulation = influences secretion

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21
Q

muscularis externa

A

three layers:
1. circular muscle
2. myenteric nerve plexus
3. longitudinal muscle

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22
Q

circular muscle

A

thick inner layer of muscularis externa
fibres oriented to cause narrowing of lumen

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23
Q

myenteric nerve plexus

A

network of nerve cells
regulate muscle function → contraction + relaxation

intrinsic neural regulation = influences smooth muscle

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24
Q

longitudinal muscle

A

thinner outer layer of muscularis externa
fibres oriented to shorten tube

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25
Q

serosa

A

connective tissue that encases intestine
connects GI tract to abdominal wall

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26
Q

blood supply to GIT

A

carries away water soluble absorbed nutrients
blood perfuses intestine → flows to liver via portal vein

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27
Q

portal circulation

A

circulation of nutrient-rich blood between the gut and liver
allows liver to remove harmful substances (filter) and process nutrients

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28
Q

portal vein

A

drains blood from digestive tract and empties directly into liver

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29
Q

liver - blood

A

receives blood from both venous and arterial circulation
receives blood that is less oxygenated but more nutrient rich than other organs

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30
Q

GI processes

A

secretion
motility

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31
Q

regulation of GI processes

A

governed by volume and composition of lumen contents

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32
Q

initiation of GI reflexes

A
  • distension of wall by volume of luminal contents
  • osmolarity of contents
  • pH of contents
  • concentrations of specific digestion contents
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33
Q

mechanoreceptor propagation

A

activated by mechanical stimuli
ex. pressure + stretch

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34
Q

osmoreceptor propagation

A

activated by changes in osmolarity

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35
Q

chemoreceptor propagation

A

activated by the binding of specific chemicals

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36
Q

enteric nervous system

A

intrinsic neural regulation

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37
Q

intrinsic neural regulation

A

controls activity of secretomotor neurons → motility + secretory function
contained within walls of GIT (short neural reflexes)
neuronal network → myenteric plexus + submucosal plexus
function independently of CNS

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38
Q

extrinsic neural regulation

A

regulation through ANS (long neural pathways)
both parasympathetic and sympathetic

influences motility + secretion of GIT
hunger, sight/smell of food, emotional state

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39
Q

parasympathetic

A

rest + digest
- stimulates flow of saliva
- stimulation of peristalsis + secretion
- stimulates release of bile

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40
Q

sympathetic

A

fight or flight
- stimulates flow of saliva
- inhibition of peristalsis + secretion

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41
Q

short reflexes

A

stimulus in lumen → receptors in GI walls → nerve plexus → target tissue → response in lumen

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42
Q

long reflexes

A

CNS → efferent autonomic neuron → nerve plexus
afferent neurons carry info from walls to CNS

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43
Q

endocrine messengers

A

hormone-secreting gland cell releases hormone → blood → distant target cells

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44
Q

neurocrine messengers

A

depolarization of nerve cells releases NT → nearby neuron/effector cell

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45
Q

paracrine messengers

A

local cell releases paracrine substances → target cells in close proximity

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46
Q

autocrine messengers

A

local cell releases substance that acts on the same cell
self-stimulating

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47
Q

hormonal control

A

chemical in lumen stimulates endocrine cell (surface exposed to lumen) to release hormones across opposite surface of cell into blood vessels in lamina propria

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48
Q

GI hormones - peptides

A

secretin
cholecystokinin (CCK)
gastrin
glucose dependent insulinotropic peptide (GIP)

feedback control system regulates aspect of lumen

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49
Q

gastrin

A

released from stomach antrum (G cells)
stimuli: peptides/amino acids in stomach; parasympathetic nerves
↑ HCl, ↑ motility in stomach, ileum, large intestine

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50
Q

secretin

A

released from small intestine (S cells)
stimuli: acid in small intestine (pH <4.5)
↓ HCl, ↓ motility in stomach
↑ HCO3-/H2O from pancreas and in bile

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51
Q

CCK

A

released from small intestine (I cells)
stimuli: digested fat/protein in small intestine
↓ HCl, ↓ motility in stomach
↑ enzymes from pancreas
↑ bile expulsion

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52
Q

GIP

A

released from small intestine (K cells)
stimuli: glucose or fat in small intestine
↑ insulin

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53
Q

motility

A

contraction + relaxation of the two outer smooth muscle layers
allows movement of contents from one site to another
peristalsis + segmentation

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54
Q

peristalsis

A

propulsion
circular muscle contracts on oral side of a bolus of food and moves towards anus = propels contents of lumen towards anus
circular muscle on other side of distended area relaxes
contraction + relaxation of longitudinal muscle is opposite of circular

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55
Q

segmentation

A

mixing
contraction + relaxation of intestinal segments
little net movement of contents towards large intestine
mixing of contents with digestive enzymes = physical breakdown
slow transit time - allows absorption of nutrients and water

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56
Q

pacemaker cells

A

throughout smooth muscle cells
constantly undergo spontaneous depolarization-repolarization cycles = slow waves
allow for propagation of electrical activity

further depolarized by excitatory hormones/NTs

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57
Q

basic electrical rhythm

A

slow waves
propagated through circular + longitudinal muscle layer through gap junctions

maintains frequency of contraction

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58
Q

slow waves in absence of neural/hormonal input

A

in fasted state
no significant contractions

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59
Q

force of contraction

A

proportional to # of action potentials fired
mediated by neuronal + hormonal input

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60
Q

phases of GI neural and hormonal control

A

classified based on site at which stimuli initiate the reflex
1. cephalic (head)
2. gastric (stomach)
3. intestinal

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61
Q

cephalic phase

A

receptors in head stimulated by sight, smell, taste, and chewing of food; emotional state

parasympathetic fibres activate neurons in the GI nerve plexi
- regulated by long reflexes

stomach: anticipatory, excitatory - via vagus nerve = release of ACh
pancreas: minor phase

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62
Q

gastric phase

A

receptors in the stomach stimulated by distension, acidity, amino acids, and peptides

short and long neural reflexes + gastrin mediate response
excitatory

stomach: major phase (excitatory via gastrin)
pancreas: minor phase (secretion stimulated by distension)

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63
Q

intestinal phase

A

receptors in intestine stimulated by distension, acidity, osmolarity, and digestive products
mediated by short + long neural reflexes and hormones: secretin, CCK, GIP

stomach: inhibitory
pancreas: major phase (acid = secretin release; digested fat + protein = CCK release)

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64
Q

lateral hypothalamus

A

feeding/hunger center
activation increases hunger
lesions = anorexia + weight loss

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65
Q

ventromedial hypothalamus

A

satiety center
activation = feeling full
lesions = overeating + obesity

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66
Q

orexigenic factors

A

increase food intake
- neuropeptide Y
- ghrelin

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67
Q

anorexigenic factors

A

decrease food intake
- leptin
- insulin
- peptide YY
- melanocortin

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68
Q

NPY

A

NT in hypothalamus
stimulates hunger

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69
Q

ghrelin

A

synthesized + released from endocrine cells in stomach during fasting
travels through blood to stimulate release of NPY in hypothalamus feeding center

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70
Q

energy intake > energy expenditure

A

↑ fat deposition = adiposites secrete leptin
= ↑ plasma leptin concentration → hypothalamus = altered activity of integrating centres (also because by inhibition of NPY release)
= reduced appetite: ↓ energy intake; ↑ metabolic rate

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71
Q

knock out leptin gene

A

mice lacking leptin will overeat and become obese
no hypothalamus feedback

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72
Q

stimulation of thirst centre in hypothalamus

A
  1. increased plasma osmolarity
  2. decreased plasma volume
  3. dry mouth and throat
  4. prevention of over-hydration
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73
Q

↑ plasma osmolarity

A

stimulate osmosreceptors in thirst centre in hypothalamus
release of vasopressin (ADH) = conservation of water at the kidney

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74
Q

↓ plasma volume

A

stimulation of baroreceptors (pressure) in cardiovascular system
baroreceptors in kidney afferent arteries activate renin angiotensin system = production of angiotensin II → hypothalamus = increase thirst

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75
Q

pairs of salivary glands

A

parotid = serous (watery)
submandibular = serous/mucous
sublingual = mucous

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76
Q

mL of saliva produced per day

A

1500 mL

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77
Q

composition of saliva

A
  1. 97-99.5% water
    - hypotonic, slightly alkaline
  2. electrolytes: rich in K+ + HCO3- ; poor in Na+ + Cl-
  3. digestive enzymes: amylase + lipase
  4. glycoproteins: mucin (mucous = mucin + water)
  5. other components like anti-microbial factors (lysozyme, lactoferrin, others)
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78
Q

functions of saliva

A

moistens + lubricates food
initiates digestion
dissolves small amount of food
antibacterial actions
aids in speech
buffering action

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79
Q

salivary glands

A

acinar cells
myoepithelial cells
ductal cells

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80
Q

acinar cells

A

leaky tight junctions = permeable

secrete initial saliva (isotonic): water, electrolyte, + protein secretion
proteins = released by exocytosis
electrolytes = Cl-, bicarbonate, K+ ions are actively secreted (transcellular)
Na+ + water follow paracellularly

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81
Q

myoepithelial cells

A

characteristics of smooth muscle and epithelial cells
contract and expel formed saliva from acinus into duct

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82
Q

ductal cells

A

tightly joined + impermeable to H2O
modify initial saliva → create alkaline + hypotonic nature

net loss of Na+ and Cl- (active reabsorption)
addition of K+ and HCO3- (active secretion)
loss > addition = hypotonic

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83
Q

regulation of salivary glands

A

no hormonal regulation

parasympathetic and sympathetic stimulate salivary secretion

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84
Q

parasympathetic regulation of salivary glands

A

↑ blood flow to glands = ↑ secretion
↑ protein secretion from acinar cells; stimulates myoepithelial cells = ↑ flow

stimulated by smell + taste; pressure receptors in mouth; nausea (protective)
inhibited by fatigue, sleep, fear, dehydration, some drugs

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85
Q

sympathetic regulation of salivary glands

A

modestly ↑ saliva flow
↑ protein secretion from acinar cells
stimulates myoepithelial cells = ↑ flow

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86
Q

starch

A

amylose + amylopectin (glucose polymers)

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87
Q

amylose

A

linear chain of glucose connected by a-1,4 linkages

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88
Q

amylopectin

A

linear chains connected by a-1,4 linkages with branched by a-1,6 linkage

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89
Q

amylase

A

initiates starch digestion in the mouth
cleaves internal a-1,4 linkages
cannot cleave ends
= maltose, maltotriose, a-limit dextrin

inhibited by acidic pH in stomach

pancreatic amylase digests majority of carbs in small intestine

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90
Q

lingual lipase

A

acid stable = active in stomach

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91
Q

conditions with impaired salivary secretion

A

congenital
Sjogren’s syndrome = autoimmune process
side effect of drugs
radiation treatment

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92
Q

impaired salivary secretion

A

dry mouth
decreased oral pH → tooth decay, esophageal erosions
poor nutrition because of difficulty swallowing foods

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93
Q

swallowing

A

complex reflex initiated by pressure receptors in walls of pharynx
stimulated by food/liquid entering pharynx

receptors send signals to centre in brainstem → signal muscles in pharynx, esophagous, respiratory muscles

peristalsis = main driving force

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94
Q

swallowing steps

A
  1. tongue pushes food bolus to back of pharynx
  2. soft palate elevates to prevent food entering nasal passages
    - swallowing centre sends impulses to inhibit resp, raise larynx, close glottis
  3. epiglottis covers glottis to prevent food/liquid from entering trachea
  4. food descends into esophagus
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95
Q

esophagus

A

transfers food from mouth to stomach
18-25 cm long
skeletal muscle surrounds upper 1/3; smooth muscle surrounds lower 2/3
food passes rapidly - no absorption; muscle glands for lubrication
specialized epithelium to protect (stratified squamous)

96
Q

upper esophageal sphincter

A

ring of skeletal muscle below pharynx

97
Q

lower esophageal sphincter

A

ring of smooth muscle at stomach

98
Q

esophageal sphincters

A

closed except when swallowing, vomiting, burping

99
Q

swallowing - esophagus

A
  1. relaxation of upper e. sphincter - food passes through, sphincter closes, glottis opens, breathing resumes
  2. peristaltic waves move food bolus down the esophagus (5-9 sec)
  3. lower sphincter opens and allows food to pass into stomach - closes once food passes through
100
Q

heart burn

A

can occur due to inefficient sphincter, after big meal, during pregnancy

101
Q

stomach

A

muscular saclike organ located between the esophagus and the small intestine
storage of food
mechanical + chemical breakdown of food
reduces food to chyme: fragments of proteins and polysaccharides, droplets of fat, salt, and water

102
Q

HCl

A

secreted by stomach
dissolves food
partially digests macromolecules
sterilization of food

103
Q

intrinsic factor

A

secreted by stomach
critical for absorption of vitamin B12 - protection from breaking down
deficiency → pernicious anemia

104
Q

vitamin B12

A

absorbed in the ileum
required for normal red blood cell formation

105
Q

fundus + body

A

thin layer of smooth muscle
secretes mucus, pepsinogen, HCl

106
Q

antrum

A

thicker smooth muscle layer
secretes mucus, pepsinogen, gastrin
grinding + mixing of food

107
Q

exocrine secretions

A

chemical messengers secreted into ducts → epithelial surface
mucous, HCl, pepsinogen

108
Q

endocrine secretion

A

chemical messengers secreted into blood
gastrin

109
Q

paracrine secretions

A

local targets
histamine + somatostatin

110
Q

gastric gland

A

mucous cells
parietal cells
chief cells
enteroendocrine cells
enterochromaffin-like cells
D cells

111
Q

chief cells

A

all regions
secrete pepsinogen

112
Q

enteroendocrine cells

A

G cell
antrum
secretes gastrin

113
Q

ECL cells

A

all regions
secrete histamine

114
Q

D cells

A

all regions
secrete somatostatin

115
Q

parietal cells

A

fundus/body
oxyntic cell
secretes HCl and intrinsic factor
have canaliculi
lots of mitochondria - acid secretion requires energy

116
Q

canaliculi

A

increase surface area of cell
maximize secretion of acid into the stomach lumen
more defined during active secretion

117
Q

acidification of stomach lumen

A

stomach secretes 2L of 0.1M HCl per day
lumen pH = 1
cytosol pH = 7

118
Q

H+/K+ ATPase

A

in luminal membrane
pumps H+ into lumen in exchange for K+ into cell
active transport
electroneutral

119
Q

carbonic anhydrase

A

catalyzes formation of H2CO3 from H2O and CO2
H2CO3 dissociates into H+ and HCO3-

120
Q

Cl-/HCO3- exchanger

A

secondary active transport
excess OH- is effluxed from the cell as HCO3- in exchange for Cl-
critical for maintenance of neutral cellular pH

121
Q

K+ channels

A

K+ recycled back into stomach lumen
diffusion
loss of positive charge

122
Q

Cl- channels

A

Cl- leaks back into stomach lumen
diffusion
compensates for loss of positive charge

123
Q

regulation of acid secretion

A

by gastrin, ACh, histamine, somatostatin
stimulation of secretion is through insertion of H+/K+ ATPase into the plasma membrane of parietal cell

124
Q

pepsinogen

A

secreted by chief cells
stimulated by ENS
parallels release of HCl
cleaved + activated to pepsin by acidic pH in stomach lumen

125
Q

pepsin

A

active only at low pH
inactivated when enters small intestine

126
Q

gastric motility

A

consumption of meal → smooth muscle relaxation mediated by PS nerves to ENS → stomach increases from 50 mL in diameter to 1.5 L without increase in pressure
food stimulates peristaltic waves

127
Q

peristaltic waves

A

weak contractions in body
powerful contraction in antrum - mixes luminal contents and causes closure of pyloric sphincter

128
Q

closure of pyloric sphincter

A

small amount of stomach contents released to duodenum
antral contents forced backwards towards body of stomach
mix contents with enzymes + acid

129
Q

vomiting

A

stimuli trigger vomiting centre in medulla oblongata
cause nausea, salivation, breath held in mid-inspiration
glottis closes of trachea
lower esophageal sphincter and esophagus relax
diaphragm and abdominal muscles contract
reverse peristalsis

130
Q

benefits of vomiting

A

removal of harmful substances prior to absorption
conditioning to prevent repeat consumption

131
Q

consequences of vomiting

A

dehydration
loss of salts → electrolyte imbalance
metabolic alkalosis due to loss of H+
acid erosion of tooth enamel

132
Q

ulcers

A

damaged/eroded area of GIT mucosa
caused by imbalance between aggressive and protective factors

133
Q

causes of ulcers

A

helicobacter pylori infection
NSAIDs decrease prostaglandin production
smoking
excessive alcohol
stress
gastrinomas

134
Q

treatment of ulcers

A

antibiotics
H+/K+ ATPase inhibitor = ↓ acid production
histamine (H2) antagonist
prostaglanding type drugs

135
Q

pancreas

A

exocrine + endocrine gland
main duct joins common bile duct from liver → enters duodenum through sphincter of oddi

136
Q

exocrine pancreas

A

produces secretions → ducts drain onto epithelial surface (apical) → into gut
source for majority of digestive enzymes → excess = lots of reserve

137
Q

HCO3- secretion

A

from pancreas (duct cells) into duodenum
watery alkaline = neutralization of stomach acid = critical for enzyme function

CFTR (Cl- channel) opens → Cl- diffusion into lumen
Cl-/HCO3- exchanged
H2O + Na+ follow paracellularly
H+/Na+ exchanged to maintain neutral pH of cytosol (carbonic anhydrase)

138
Q

endocrine pancreas

A

produces hormones - regulation of entire body
ductless gland
secretion occurs across epithelial basolateral surface for diffusion into blood

139
Q

pancreatic ducts

A

acinar cells - produce and secrete digestive enzymes through exocytosis
duct cells secrete H2O and HCO3-

140
Q

pancreatic juices

A

isotonic (Na+, K+ = in plasma)
alkaline (high HCO3-, low Cl-)
1-2 L/day
electrolytes + digestive enzymes

141
Q

proteolytic enzymes

A

stored + secreted in inactive forms
activated in duodenum
prevent autodigestion

142
Q

tide

A

what goes into blood
parietal cells (stomach) = alkaline tide
duct cells (pancreas) = acid tide

143
Q

proteases

A

digest proteins into peptides + amino acids

144
Q

amylolytic enzymes

A

amylase (secreted in active form)
digest starch into sugars by a-1,4 cleavage = maltose, maltotriose, a-limit dextrins

145
Q

lipase

A

active enzyme
digest triglycerides into free fatty acids + 2-monoglycerides

146
Q

nucleases

A

digest nucleic acids into free nucleotides

147
Q

pancreatic acinar cells

A

synthesize + package pro-enzymes into zymogen granules → stored at apical pole of cell until stimulation
neurohormonal input results in exocytosis

148
Q

enterokinase

A

enzyme embedded in luminal membrane of duodenum
cleaves trypsinogen to trypsin

149
Q

trypsin

A

active form of trypsinogen; activated by enterokinase
protease - endopeptidase = hydrolysis of interior peptide bonds of proteins + polypeptides
activates other proteases

150
Q

prevention of autodigestion

A
  1. digestive enzymes are stored as inactive proforms → only activated once they reach intestine
  2. pancreas secretes trypsin inhibitors in case of any premature activation
  3. trypsin has intrinsic properties to self-degrade if activated before intestine
151
Q

cystic fibrosis

A

mutation of CFTR Cl- channel in pancreas
pancreas insufficiency
normal production of digestive enzymes but minimal secretion of HCO3- + H2O secretion = enzymes don’t reach intestine → autodigestion of pancreas = inflammation

require supplements of enzymes for adequate nutrition

152
Q

chymotrypsin

A

active form of chymotrypsinogen
activated by trypsin
endopeptidase = hydrolysis of interior peptide bonds of proteins + polypeptides

153
Q

elastase

A

active form of pro-elastase
activated by trypsin
endopeptidase = hydrolysis of interior peptide bonds of proteins + polypeptides

154
Q

carboxypeptidase A & B

A

active form of pro-carboxypeptidase A & B
activated by trypsin
exopeptidase = hydrolysis of bonds at C-terminal ends

155
Q

phospholipase A2

A

active form of prephospholipase A2
activated by trypsin
hydrolysis of phospholipids → free fatty acids + lysophospholipids

156
Q

cholesterolesterase

A

active enzyme
hydrolysis of cholesterol-esters → free fatty acids + cholesterol

157
Q

CCK secretion

A

fatty acids + amino acids in small intestine trigger CCK secretion from cells in small intestine into blood

158
Q

CCK stimulates:

A

pancreas - increase digestive enzyme secretion
gall bladder contraction - release of bile acids for fat breakdown + relaxation of sphincter of Oddi

= absorption of fat and amino acids
removal stops CCK release = negative feedback

159
Q

secretin secretion

A

triggered by reduced pH as acid enters duodenum from stomach
enteroendocrine cells in small intestine → blood

160
Q

secretin stimulates

A

pancreas + liver duct cells to increase HCO3- secretion

negative feedback when stomach acid is neutralized

161
Q

secretin + CCK inhibit gastrin secretion

A

↓ gastrin =
- reduced stomach motility (slowed emptying)
- reduced acid secretion

162
Q

liver

A

largest internal organ
receives 25% of cardiac output
~2.5% of body weight
extends across entire abdominal cavity (mostly RUQ)

163
Q

hepatic lobule

A

hexagonal structure
central vein through centre
portal triads at each corner

164
Q

portal triad

A

branches of
- portal vein
- hepatic artery
- bile duct

165
Q

liver epithelial cells

A

hepatocytes (70% of liver cells)
cholangiocytes (3-5% of liver cells)

166
Q

cholangiocytes

A

bile duct epithelium cells

167
Q

Kupffer cells

A

liver macrophages

168
Q

liver endothelial cells

A

line sinusoids
fenestrated = gaps in between cells → leaky

169
Q

bile canaliculi

A

tube like structures where hepatocytes join
drain into bile ducts

170
Q

functions of liver

A

exocrine gland (bile)
metabolism + storage of nutrients
deactivation + detoxification of harmful substances
production of circulating proteins

171
Q

bile

A

emulsification + digestion of fats

constituents
- bile acids
- cholesterol
- salts + water
- phospholipids
- bile pigments
- trace metals

172
Q

fat digestion

A

emulsification of fat globule
digestion by pancreatic lipase

173
Q

emulsification

A

requires
- mechanical disruption (GI motility) → make lipid droplets smaller (↑ surface area)
- emulsifying agent prevents re-aggregation

174
Q

emulsifying agents

A

amphipathic bile acids
phospholipids

175
Q

mixed micelles

A

soluble cluster of amphipathic molecules - nonpolar groups in middle + polar groups on outer layer (single, not bilayer)
formed by bile acids + phospholipids + lipase digestion products

keep monoglycerides + fatty acids in small soluble aggregates
“holding station” for small nonsoluble lipids

176
Q

formation of bile

A

hepatocytes produce + secrete bile acids, phospholipids, cholesterol, bile pigments into canaliculi (across apical membrane)
components secreted through primary active transport pathways

bile duct cells add HCO3- + salts + H2O → bile flows into larger ducts

177
Q

gallbladder

A

stores + concentrates the bile between meals
expelled into duodenum after a meal

178
Q

enterohepatic circulation of bile acids

A

recycling

20-40g of bile acids are released into intestine every day
0.5g lost in feces = 95% recovered

allows secretion rate to exceed synthesis rate

179
Q

bile acid recycling

A
  1. bile acids are released by liver/gallbladder into duodenum for fat digestion
  2. reabsorbed across ileum into portal circulation
  3. transported back into hepatocytes
180
Q

fibre

A

↓ efficiency of recycling = bile acid lost in feces
use cholesterol stores to synthesize more bile acids = ↓ plasma cholesterol

181
Q

enterohepatic circulation of drugs/toxins

A

beneficial: loperamide (target gut)
disadvantage: reduced bioavailability

182
Q

hepatobiliary secretion

A

regulated during intestinal phase
secretin: produced + released by S-cells in duodenum → increases HCO3- secretion by bile duct cells
CCK: produced by I cells in duodenum + jejenum → increases gallbladder contraction + relaxation of sphincter of Oddi = release of bile into duodenum

183
Q

gallstones

A

cholesterol stones: [cholesterol] > [bile acids] = precipitation in gallbladder; requires “nucleating” agent like protein or bacteria to bind to

pigment stones: less common; excessive hemolysis = ↑ [bile pigment] in bile → precipitation with Ca2+

184
Q

gallstones consequences

A

depends on location
obstruction/infection of gallbladder, liver, pancreas
pain, nausea, jaundice, malabsorption of fats + fat soluble vitamins

185
Q

gallstone treatment

A

cholecystectomy = removal of gallbladder
removal of stones
drugs to dissolve gallstones

186
Q

small intestine

A

between stomach + large intestine
2.4 cm diameter; 3m length
duodenum ~30 cm
jejunum ~1m
ileum ~1.7m

digestion + absorption of protein, fat, carbs, electrolytes, water, minerals, vitamins

187
Q

duodenum

A

receive from pancreas, liver, + stomach
mixing of pancreatic digestive enzymes + bile with food
absorption of nutrients, iron, + calcium
release of endocrine hormones: secretin + CCK

188
Q

jejenum

A

digestion + absorption

189
Q

ileum

A

digestion + absorption continue
recycling of bile acids
absorption of vitamin B12

190
Q

folds of Kerckring

A

circular folds
infolding of inner wall of s. intestine
↑ surface area

191
Q

sloughed cells

A

tips of villi cells that are digested and absorbed

192
Q

absorptive cells

A

absorption from lumen
brush border enzymes

193
Q

goblet cell

A

secretion of mucus across apical surface into lumen
protection from stomach acid

194
Q

enteroendocrine cell

A

release of hormones across basolateral surface into ISF
S cells - secretin
I cells - CCK

195
Q

paneth cell

A

secrete antibacterial proteins across apical surface into lumen

196
Q

brush border

A

microvilli = small projections of epithelial cells covering villi of small intestine
major absorptive surface

197
Q

brush border enzymes

A

have membrane domain (anchored to brush border) + catalytic domain (in lumen - catalytic activity)
important for breaking down carbohydrates and peptides into sugars and amino acids before transport across enterocyte

sucrase, maltase, lactase

198
Q

carbohydrate digestion

A

maltase, sucrase, a-dextrinase: maltose / maltotriose → glucose

a-dextrinase: a-limit dextrins → glucose

sucrase: sucrose → glucose + fructose

lactase: lactose → glucose + galactose

199
Q

SGLT

A

Na+dependent glucose transporter
secondary active transport
moves 2 Na+ and glucose/galactose into cell

200
Q

GLUT2

A

facilitative carrier
moves glucose/galactose + fructose into capillaries

201
Q

GLUT5

A

facilitative carrier
moves fructose into cell

202
Q

lactose intolerance

A

too much loss of lactase
results in decreased water absorption in the gut (osmotic gradient) → lactose-containing fluid is digested by bacteria in the large intestine

203
Q

protein digestion

A

in stomach by pepsin
in small intestine by pancreatic proteases (trypsin + chymotrypsin)

204
Q

free amino acids

A

result of protein digestion by carboxypeptidase, aminopeptidase + other brush border enzymes
absorbed by secondary active transport coupled to Na+

peptidases in cytosol hydrolyzed small peptides into amino acids

undergo facilitated diffusion across basolateral surface of enterocyte

205
Q

fat absorption in enterocyte

A

fatty acids + monoglycerides are processed by ER into triglycerides (maintains diffusion gradient)
aggregate into lipid droplets coated with amphipathic proteins → packaged in the golgi + secreted via exocytosis

206
Q

chylomicrons

A

extracellular fat droplets
contain triglycerides, phospholipids, fat soluble vitamins, + cholesterol

207
Q

lacteals

A

lymphatic vessels - leakier than capillaries
large chylomicrons enter into lymphatic system → pass through thoracic duct into systemic circulation

208
Q

lipoprotein lipase

A

on endothelial cells lining blood vessels
release triglycerides from chylomicrons as monoglycerides + free fatty acids → taken up by tissues + used for energy

209
Q

absorption of iron

A

Fe2+ is actively transported into enterocyte by DMT-1 → incorporated into protein ferritin

released on basolateral side by ferroportin
transported through blood attached to transferrin (plasma protein)

210
Q

ferritin

A

protein iron complex that acts as a storage form of iron

211
Q

excretion of iron

A

stored in enterocyte → excreted when villi tips are sloughed off

in body: no mechanism of excretion → accumulation in tissues (can lead to toxicity)

212
Q

high iron stores

A

upregulation of ferritin expression
= reduced absorption of iron

213
Q

depleted iron stores

A

deficiency
downregulation of ferritin production = increased absorption

214
Q

iron deficiency anemia

A

reduced number/size of RBCs
symptoms: tiredness, light-headedness, headaches
caused by iron-deficient diet, blood loss, poor iron absorption

215
Q

control of fluid in intestine

A

critical for GI function
- contact between food and digestive enzyme
- diffusion of digested nutrients to absorption site
- fluidity provides transit without damage to epithelium

216
Q

amount of fluid

A

8-9L handled by GI tract per day
~7L reabsorbed in small intestine
~1.5L absorbed into blood by large intestine
100 mL lost in feces

217
Q

water absorption/secretion in s. intestine

A

absorption at villi
- depends on Na+ gradients generated during secondary active nutrient uptake

secretion from crypts
- depends on Cl- gradients generated by NKCC1
cAMP necessary to signal opening of Cl- channels - Na+ + H2O follow efflux

218
Q

osmotic gradient

A

established by intestinal epithelium
water follows through tight junctions (paracellular transport)

219
Q

NKCC1

A

secondary active transporter
Na+/K+/2Cl- move into cell from blood

220
Q

cholera

A

contamination of food/water by vibrio cholerae bacteria → produce toxin that increases cAMP production in crypt epithelium of small intestine = Cl- channel stays open + excessive secretion of Cl- into gut lumen
vomiting + excessive diarrhea leads to dehydration, electrolyte imbalance

221
Q

segmentation in small intestine

A

continuous division + subdivision of intestinal contents
increases surface area of food + mixes with digestive enzymes
frequency of contraction set by basic electrical rhythm
contraction force determined by neurohormonal input

slow net migration towards large intestine

222
Q

basic electrical rhythm in small intestine

A

12 contractions/min in duodenum
9 contractions/min in ileum

223
Q

migrating myoelectric complex

A

pattern of peristaltic activity that replaces segmentation when contractions stop after absorption
begins in antrum →travels ~2ft + dies out
overlapping waves = ~2hrs to travel along small intestine; then repeats

pushes undigested material to large intestine
prevents bacteria from remaining in small intestine

224
Q

motilin

A

intestinal hormone released by cells in small intestine
initiates MMC = regulation

feeding inhibits release of motilin → prevents peristalsis when absorption is needed
MMC ceases when next meal is consumed

225
Q

large intestine

A

diameter = 6.5 cm (large)
length = 1.5 m (shorter than small intestine)
no villi, only crypts

ascending → transverse → descending → sigmoid colon
functions:
- reabsorption of water
- reservoir for storage of wastes and indigestible materials prior to elimination by defecation
- absorption of products of bacterial metabolism

226
Q

ileocecal valve

A

sphincter between cecum and ileum
opens when ileum contracts post-meal
closed when large intestine is distended
retains large intestine contents including bacteria

227
Q

cecum + appendix

A

no apparent function in humans
some species: well developed, contains commensal bacteria important for complex carbohydrate digestion

228
Q

rectum

A

reservoir for feces

229
Q

anus

A

two sphincters that control defecation
external anal sphincter = skeletal muscle
internal anal sphincter = smooth muscle

230
Q

cells of large intestine

A

stem cells in crypts differentiate into four epithelial cell types
- absorptive cells (enterocytes) - no brush border enzymes
- goblet cells - abundant
- paneth + endocrine cells - very few

231
Q

gut microbiome

A

bacterial ecosystem in large intestine
>1000 species
liberate short chain fatty acids from dietary fibre → then absorbed
produce vitamins (vit K) that are absorbed
population influenced by diet, medications, + bowel function

232
Q

absorption of water in large intestine

A

upper portions of crypts
depends on Na+ gradients generated by Na+/K+ ATPase
Cl- + H2O follow ↑[Na+] in blood

233
Q

secretion of water in large intestine

A

identical to small intestine
depends on Cl- gradients generated by NKCC1
Na+ + H2O follow ↑[Cl-] in lumen

234
Q

NKCC1

A

secondary active Na+/K+/2Cl- transporter

235
Q

motility of large intestine

A

mixing of contents + retention for salvage of fluid + bacterial products
segmentation → 1/30 min (slower basic electrical rhythm)
contents retained in colon for 18-24 hrs

propulsion: intense contraction (mass movement) 3-4x/day pushes contents to anus
after eating + prior to defecation

236
Q

feces

A

water
undigested food
bacteria
sloughed epithelial cells

237
Q

defecation

A

initiated by mass movement in large intestine
rectum distends → activation of mechanoreceptors
reflex: rectum contracts, internal anal sphincter relaxes + external sphincter contracts
increased peristaltic activity in sigmoid colon = ↑ pressure → reflex relaxation of external anal sphincter
(reflex can be over-ridden by brain to delay relaxation of external sphincter → reverse peristalsis = move contents back into sigmoid colon)

Physiology (12 decks)

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