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GI- Week 1 > Prunuske: GI Function and Physiology > Flashcards

Prunuske: GI Function and Physiology Flashcards

1
Q

What is a bolus?

A

rounded mass of food ready to swallow

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2
Q

What is borborygmi?

A

abdominal rumbling sounds

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3
Q

What is chyme?

A

semifluid mass of partly digested food passed from the stomach to the duodenum

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4
Q

What is the diverticulum?

A

Outpouching of GI wall

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5
Q

What is eructation?

A

Belching

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6
Q

What is peristalses?

A

Propulsion of food through the esophagus and intestines

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7
Q

What is posprandial?

A

After feeding

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8
Q

What is sitophobia?

A

fear of eating

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9
Q

What is steatorrhea?

A

fatty stools

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10
Q

heptao

A

liver

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11
Q

eopha

A

esophagus

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12
Q

cholecyst

A

gallbladder

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13
Q

gastro

A

stomach

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14
Q

colo

A

large intestine

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15
Q

ileo

A

small intestine

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16
Q

What structures are in the upper GI tract?

A 
oral cavity
pharynx
esophagus
stomach
sml intestine
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17
Q

What structures are in the lower GI tract?

A

large intestine

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18
Q

What are the gross structures of the small intestine?

A

duodenum
jejunum
ileum

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19
Q

What are the gross structure of the large intestine?

A

cecum
colon
rectum
anus

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20
Q

What are the accessory organs of the GI system?

A 
Salivary glands (parotid, submandibular, sublingual)	Exocrine Pancreas 	
Liver- Hepatic system	Gallbladder- Biliary system
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21
Q

What regulates movement in the GI tract and allows some compartments to act as reservoirs?

A

sphincters

UES
LES
Pylorus
SOO
Ileocecal valve
Internal and external anal sphincters
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22
Q

What sphincters can you voluntarily control?

A

External Anal sphincter

UES

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23
Q

What is the purpose of mucosal folding? How do villi differ between the small intestine and the colon?

A

increases SA

Sml intesetine- villi + crypts
Colon/stomach- flatter + crypts

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24
Q

How are GI cells unique from other cells?

A

They undergo constant renewal!

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25
Q

Describe how GI cells are renewed.

A

STEM cells at the base of the crypts divide, differentiate and migrate to the tips of the villi

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26
Q

How often are GI cells shed and why is this important

A

Apoptosis occurs every 3-6 days and sheds cells into the lumen

Prevents the accumulation of mutations d/t toxin exposure

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27
Q

What are the 4 major layers of the GI wall?

A

Mucosa
submucosa
muscularis externa
serosa

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28
Q

What is a diverticulum?

A

Single pouch protruding from an alimentary tract (usually false)

True- includes all 4 layers
False- includes serosa and mucosal layer

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29
Q

Why is it important to have fiber in your diet?

A

Lack of fiber can lead to diverticulosis which means you have multiple diverticula, which can progress to diverticulitis…which is bad.

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30
Q

What secretes mucus in the GI tract?

A

goblet cells!

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31
Q

What is MUCIN?

A

It’s a protein that makes mucus!!

protein monomers combined into complexes by disulfide links

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32
Q

How many layers of mucin are there in the stomach and colon vs the small intestine?

A

2 layers in the stomach and colon, 1 layer in small intestine

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33
Q

What protects the protein core of mucin from proteases?

A

glycosylation (sugar groups prevent sequence specific recognition by proteases)

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34
Q

What is coated w/ transmembrane mucins?

A

enterocytes

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35
Q

What are the 4 basic processes facilitating caloric uptake?

A

Digestion, absorption (excess capacity)

Secretion, motility (under nerual/hormonal control)

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36
Q

How do you make a bolus?

A

TEETH masticate food and SALIVA provides lubrication and AMYLASE to create a bolus

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37
Q

How do you make chyme?

A

Stomach movements +
pepsin further digests food>
chyme

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38
Q

What type of enzymes does the duodenum contain and what gives it additional digestive enzymes?

A

brush border enzymes

pancreas

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39
Q

Where does most abosrption occur?

A

villi (gives small intestine more SA)

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40
Q

What transports nutrients and ions?

A

Enterocytes–> CAPILLARIES (transport the absorbed nutrients)

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41
Q

What transports most fats to the lymph?

A

Lacteals (TOO BIG TO ENTER CIRCULATORY SYSTEM)

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42
Q

What is absorption?

A

Transport of nutrients across epithelium into blood or lymphatic system

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43
Q

Where are AA, monosaccharides and lipids absorbed?

A

Duodenum

Jejunum

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44
Q

What helps to facilitate hte absorption of lipids?

A

Bile salts from the LIVER that act as DETERGENTS

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45
Q

Where are cobalamine (B12) and bile salts/acids absorbed?

A

usually the ileum– need to be recycled so you have enough to coat a fat molecule

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46
Q

Where are water and electrolytes absorbed?

A

small and large intestines

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47
Q

What does absorption depend on?

A

Splanchnic circulation (all the blood vessels in the gut)!

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48
Q

What is normal blood lfow?

A

1 to 5 liters/min depending on regulators of vasomotor tone

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49
Q

At rest, how much blood flow goes to the gut?

A

21% (gut is about 5% of body mass)

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50
Q

Where does all blood flow leaving the intestines go? Why?

A

Intestine>
portal vein>
LIVER>
DETOXIFICAITON

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51
Q

Blood supply to the liver comes from….

A 
hepatic artery (1/4 of blood)
portal vein (3/4 of blood)
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52
Q

What happens to blood flow to the gut when it’s really active?

A

it increases 4-5 fold

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53
Q

What happens to blood flow to the gut during exercise and emergency situations?

A

vasoconstriction SHUNTS blood away

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54
Q

Is it a bad idea to swim after eating?

A

Only after consuming alcohol.

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55
Q

What is enterohepatic circulation?

A

Recycling of bile salts/acids through the hepatic portal vein

  • don’t need to synthesize as many new bile ducts
  • some drugs/bacteria can modify bile salts and make them less easier to reabsorb
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56
Q

What are the metabolic vasodilators that increase blood flow?

A

CO2
H
K
adenosine

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57
Q

What can alter blood flow in the gut?

A

autonomic and enteric neural influence

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58
Q

What happens to chylomicrons?

A

Too large to pass through capillary cells SO they’re absorbed by LACTEALS which empty in to the bloodstream via the THORACIC DUCT

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59
Q

What are the causes of mesenteric ischemia?

A
  1. occlusive mechaisms (thrombi, mesenteric infarction)
  2. non-occlusive mechanisms- prolonged reflex vasoconstriction (hypovolemia, HF) or abnormal levels of circulating vasoconstrictors (Epi, Ang II)
60
Q

How does a pt who has had a mesenteric infarction present clinically?

A

Post prandial pain

Sitophobia (fear of eating)

61
Q

What has happened on a physiological level to a pt w/ mesenteric infarction?

A

Necrosis of the tips of the villi>

Loss of barrier function of the wall of the gut and uptake of vasodilator toxins from gut> SEPTIC SHOCK

62
Q

Why is a fluid environment vital to the GI system?

A

supports uptake of nutrients and minimizes DAMAGE to epithelium

63
Q

What supplies fluid to the GI tract?

A

Organs that drain into the GI tract

GI epithelial cells

64
Q

What does fluid in the GI tract contain?

A

ions
digestive enzymes
mucins
bile

65
Q

What happens to the majority of fluids?

A

reabsorbed in the small intestine w/ nutrients

66
Q

What regulates secretion?

A

parasympathetic
hormonal
enteric nerves

67
Q

What is transmural water movement?

A

Water moves across the epithelium driven by PRESSURE created by OSMOTIC gradients

a) THROUGH CELLS (transcellular route) perhaps with the help of specific water channels (aquaporins)
b) BETWEEN CELLS (paracellular route) according to osmotic gradients driven by active electrolyte transport

68
Q

What affects conductivity (leakiness) in the GI tract?

A

Presence or absence of tight jxns

69
Q

What mediates fluid uptake in the small intestine?

A

absorption of NUTRIENTS in the small intestine (SGLT-1)

70
Q

What is diarrhea?

A

an increase in water in the lumen

71
Q

What is osmotic diarrhea?

A

small bowel overgrowth (bacteria/defect in digestion of carbs)>
increased production of ORGANIC ACIDS in the LUMEN>
pulls water from blood stream by OSMOSIS

72
Q

What causes secretory diarrhea?

A

infection leads to EXCESS secretion of Cl drawing water INTO the lumen

73
Q

What are the effects of diarrhea?

A

(When 8.5 L aren’t absorbed)

dehydration
electrolyte imbalance
metabolic disturbance

74
Q

What affects fluid flux?

A

SA available for ion transport

Residence time in the lumen
-decrease transit time and INCREASE absorption

75
Q

How does loperamide work?

A

Antidiarrheal

SLOWS transit to increase fluid absorption

76
Q

What controls the length of time for digestion and absorption?

A

motility

77
Q

What is the average transit time in the esophagus, stomach, SI and LI?

A

10 s
4-5 hrs stomach
2.5-3 sml intestine
30-40 lg intestine

78
Q

What is most of the GI tract composed of?

A

Smooth muscle (long slender cells separated into branching bundles and covered by CT)

79
Q

Where is striated muscle in the GI tract located?

A

esophagus
pharynx
external anal sphincter

80
Q

What are gap junctions or nexuses in smooth muscle?

A

low ressistance electrical coupling between cels to enable the conteracation wave to spread to adjacent cells

81
Q

What modulates activity/frequency of the smooth muscle/gap junctions?

A

NT released form intermittent swellings along the nerve axon

82
Q

What is the difference between a phasic and a tonic contraction?

A

Phasic (s)

TONIC contractions (min to hrs)–> most important at sphincters

83
Q

How is basal resting tension or TONE in GI smooth muscle maintained?

A

WIHTOUT elevation of intracellular Ca and WITHOUT energy expenditures (sphincters)

84
Q

How much can GI smooth muscle shorten by?

A

50%

85
Q

What stimulates GI smooth muscle to contact?

A

Stretch>

depolarization

86
Q

What are sphincters?

A

one way valves

87
Q

What causes relaxatin of a sphincter?

A

proximal pressure

88
Q

What causes contraction of a sphincter?

A

distal pressure

89
Q

What initiates slow wave electrical activity in GI smooth muscle?

A

Interstitial cells of cajal initiate then
propagated over a few cm

PHASIC

90
Q

What causes slow wave generation in GI smooth muscle?

A

Increase in Ca followed by repolarization by K channels

91
Q

How do you alter the AMPLITUDE (not the frequency) of the slow waves?

A

signals releasing calcium from internal stores or opening Ca++ channels on plasma membrane

92
Q

What initiates excitation contraction coupling in smooth muscle cells?

A

Increase in intracellular Ca ion concentration

93
Q

Describe the pathway for contraction of GI smooth muscle.

A

ACh binds MR>
increased influx of Ca into cell>
activation of calmodulin-dependent myosin light chain kinase>
phosphorylation of myosin>
increased myosin ATPase activity and binding of myosin to actin>
contraction

94
Q

What are peristatltic contractions?

A

Propel intestintal contents FORWARD

95
Q

What are segmenting contractions?

A

contractions of circular muscles in small and

large intestine that locally mix contents (churning), nonpropulsive

96
Q

What is the migrating motor complex?

A

relaxation of sphincters and contractions in stomach and small intestine occurring during fasting controlled by hormone MOTILIN

97
Q

Does it take 7 years to digest gum?

A

NO migrating motor complex helps clear things out that we’re not able to digest

98
Q

What is the mini brain of the gut?

A

enteric nervous system (100 million neurons)–> can act alone to mediate short reflexes INDEPENDENT of input from the CNS

(Submucosal and Myenteric nerve plexuses)

99
Q

Where is the submucosal nerve plexus located?

A

SMALL and LARGE intestine

location: submucosa
fxn: sensory and regulates blood flow,

Meissner’s

100
Q

What is the myenteric nerve plexus?

A

between circular and longitudinal muscle layer from esophagus to internal anus

Auerbach’s

101
Q

What detects changes in the GI tract?

A

intrinsic sensory receptors:

stretch receptors, osmoreceptors, and chemoreceptors

102
Q

Activation of receptors in the GI tract leads to…

A

release of signaling molecules or upregulation of transporters

103
Q

Do chemosensitive taste receptors always evoke taste?

A

NO, but they do localize to multiple spots in the body!

104
Q

What does enteric nervous system consist of?

A

afferent sensory neurons

105
Q

What excites the afferent sensory neurons of the gut?

A
  1. fast distension of the gut

2. chemical signals from the lumen

106
Q

What stimulates the sensory neurons?

A

serotonin (5HT) released form ECL (monitor what’s going on)

–>respond w/ a few AP followed by hyperpolarization/adaption after a while

107
Q

What do the afferent sensory neurons do?

A

transfer information about gut environment to INTERNEURONS in myenteric plexus which relay signals up and down the gut

108
Q

Where are efferent motorneurons primarily found?

A

Myenteric plexus

109
Q

What type of structure do efferent motor neurons have? What excites them? How do they respond?

A

uniopolar

fast EPSPs

sustained trains of APs

110
Q

What organs do efferent motorneurons affect?

A

carry “efferent” information to GI smooth muscle, vascular smooth muscle, GI exocrine secretory cells and GI endocrine secretory cells

111
Q

What is the the difference between excitatory and inhibitory fibers that affect efferent motorneurons?

A

Excitatory fibers release acetylcholine, neurokinin A and substance P

Inhibitory fibers release vasoactive intestinal peptide (VIP) and nitric oxide (NO) on smooth muscle cells.

112
Q

Short neural reflexes affecting GI function involve…

A

nerves of the enteric plexus

113
Q

Long neural reflexes affecting GI funciton involve…

A

both CNS and ANS

114
Q

_________ activate both autonomic nervous system and enteric nervous system promoting secretion and motility.

A

Nutrients

115
Q

How does being a quadraplegic (w/out higher center) affect your GI control?

A

GI can operate fine, but control of secretion and motility may be less than optimal

116
Q

Afferent information leaving the GI tract is carried by….

A

the Extrinsic autonomic nervous system

117
Q

How does parasympathetic activity affect the GI tract? Through which nerve?

A

Stimulates activity of the enteric plexuses, increases GI MOTILITY and SECRETORY activity.

REST AND DIGEST

Cholinergic of VAGUS nerve

118
Q

How does sympathetic activity affect the GI tract? through which nerve?

A

INHIBITS activity of the enteric plexuses, decreases GI motility, contracts GI sphincters, constricts GI microvasculature

mostly adrenergic

119
Q

What is the difference between parasympahetic activity and sympathetic activity on contractile waves?

A

parasympathetic increases activity, cholinergic, vagus
“rest and digest”

  • sympathetic stimulation decreases activity. EPINEPHRINE
120
Q

What is the vago-vagal reflex?

A

Vagal afferent info is transmitted to autonomic centers in the medulla

Vagal efferents coordinate excitatory and inhibitory activity within the Enteric Nervous System to mediate peristalsis

121
Q

ACh

A

the primary EXCITATORY transmitter from sensory cells and from motoneurons to muscle, epithelium, secretory cells and at interneuronal junctions.

INCREAES INTRACELLULAR Ca++

  • can also cause release of NO/VIP which is inhibitory
122
Q

Gastrin release peptide (GRP)

A

released from vagal nerve endings to stimulate G cell secretion of GASTRIN

GASTRIC ACID SECRETION

123
Q

Substance P (tachykinin)

A

an EXCITATORY transmitter generally co-released with acetylcholine

124
Q

Vasoactive intestinal peptice (VIP)

A 
Promotes motility (FORWARD MOVEMENT)
RELAXES smooth muscle in esophagus and stomach

Stimulates fluid secretion and promotes dilation of the GI vasculature. INCREASES cAMP

**IMPT in relaxing tonically active sphincter

125
Q

NO

A

an inhibitory transmitter co-release with VIP from inhibitory motoneurons, hydrophobic- intracellular targets

126
Q

Gastrin

A

G cells in antrum of stomach detect AA leading to PEPSINOGEN and H+ release from parietal cells

127
Q

Choleocystokinin (CKK)

A

As cells move from stomach to sml intestine:

I cells in D/J detect FAT and AA>
secretion of PANCREATIC ENZYMES and BILE SALTS

involved in fat uptake

128
Q

Secretin

A

Duodenum/jejunum region:

S cells primarily in D/J detect ACID stimulates secretion of BICARBONATE (pancreas) and inhibits gastric motility

129
Q

Gastric Inhibitory Peptide or Glucose Dependent Insulinotropic Peptide (GIP

A

K cells in D/J detect CARB and FAT to inhibit gastric acid secretion and stimulate INSULIN release from pancreas.

130
Q

Motilin

A

secreted by endocrine cells; released cyclically during FASTING STATE to initiate Migrating Motor Complex

131
Q

Portal blood concentration of which substance will increase when the lumen of the small intestine is perfused with a buffered solution of pH3?

A

Secretin

132
Q

What are paracrine regulators?

A

Histamine (ECL cells)

Somatostatin (D cells)

133
Q

Where does synthesis of secretions occur?

A

In specialized cells and products are packaged into ZYMOGEN granules and stored

134
Q

What stimulates secretion?

A

stimulus-induced increase in either cAMP or [Ca+2]i (or both) … which then leads to zymogen granule docking and dumping

135
Q

What is the forgotten organ of the gut?

A

Microbiota

Human body 10^13 cells

Gut 10^14 microorganisms (500 different species, mostly ANAEROBES- difficult to culture) and quadrillion viruses

The lumen of the gut is equivalent to being outside the body

Regional and developmental variability

Create physiological inflammation within GI track

Reside in outer mucus layer of the large intestine

Constitute 60% of fecal mass

Changes in microbiota are associated with obesity and inflammatory diseases

136
Q

What causes burping?

A

Air swallowed during eating is released by eructation

137
Q

What generates CO2 in the gut?

A

neutralization of gastric acid by bicarb

138
Q

Femermentation of fiber in the colon can lead to gas byproducts. What can use these byproducts in the gut?

A

Bacteria
Excreted by the lungs
evacuated

139
Q

What is borborygmi?

A

Movement of gas in the BOWELS not stomach

140
Q

Why are some people’s flatulence flammable?

A

Methane

Only some people have the methanobrevibcter smithii in their microbiome

141
Q

What can cause bacterial overgrowth syndrome?

A

Delayed small intestine transit and diverticulum

-gas and bloating from fermentation

142
Q

How can bacterial overgrowth syndrome lead to anemia?

A

bacteria compete for B12 uptake

143
Q

How can bacterial overgrowth syndrome lead to steatorrhea?

A

Deconjugate bile acids

144
Q

How do you diagnose bacterial overgrowth syndrome?

A

Hydrogen breath test

145
Q

What are properties of hte gut that limit colonization by microorganisms?

A

Saliva contains lactoferrin, lysozyme, and secretory IgA
Acidic environment in stomach
More lymphocytes in GI than the circulating immune system
Mucus- IgA, lysozyme, lactoferrin
Paneth cells secrete antimicrobial peptides
Digestive enzymes cleave bacteria
Diarrhea
Vomiting
Microflora prevent colonization of pathogenic microorganisms (probiotics and prebiotics, <pH)
Peristalsis, Ileoceccal valve

GI- Week 1 (12 decks)

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