GI Flashcards

1
Q

Lumen

A

Cavity where food travels from mouth to anus and secretions from various organs drain

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2
Q

Blender

A

Stomach, stays for at least 4 hours

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3
Q

Reaction vessel

A

First part of small intestine, enzymes from pancreas neutralize acid, detergent is bile from liver

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4
Q

Residue combuster

A

Where feces are formed

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5
Q

Mouth

A

Mechanical shearing of ingested food, grinding to reduce size of food particles, saliva added

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6
Q

Saliva

A

Moistens to taste, signifiant amount of enzymes, lubricates food bolus to allow swallowing, begins digestion of carbohydrates and lipids

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7
Q

Esophagus

A

Transfers food to stomach by peristaltic waves, moves actively (without gravity), flexible tube with sphincter at each end

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8
Q

Lower esophageal sphincter

A

Opens as soon as food is swallowed, and opens until food enters your stomach
Begins stomach
Tonically contracted

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9
Q

Stomach

A

Begins with lower esophageal sphincter, 3 sections
1. Fundus
2. Body
3. Antrum
Exits antrum to small intestine through pyloric sphincter
Can also be divided into orad and caudad region
Stores food in upper stomach
Specialized cells secrete mucous, enzyme precursors, hydrochloric acid and hormones
Grinding occurs in lower stomach

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10
Q

Chyme

A

Enters small intestine from stomach, pretty liquid: delivered to duodenum

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11
Q

Small intestine

A
4-6 meters long
1. Duodenum
2. Jejunum
3. Ileum
Absorption of nutrients occurs mostly in jejunum and ileum
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12
Q

Duodenum

A

Very short

Secretions from pancreas and liver via pancreatic and common bile ducts

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13
Q

Jejunum

A

40% of small gut

Larger diameter, thicker wall, more prominent circular folds, less fatty mesentery

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14
Q

Mesentery

A

Connects small intestine to wall and important in blood circulation

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15
Q

Ileum

A

60% of small gut
Empties into large intestine
Hard to say border between jejunum and ileum
Thinner than jejunum

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16
Q

Large intestine (colon)

A

Re-absorbs water used in digestion process, starts at cecum and ends at anus

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17
Q

Appendix

A

No function in humans

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18
Q

Villi

A

Fingerlike extensions that face lumen of tract, increase surface area of small intestine
Microvilli project outwards to form brush border

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19
Q

Crypt

A

Colon

Structurally and functionally different from villi

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20
Q

Three major salivary glands

A
  1. Parotid gland (large, behind ear)
  2. Submandibular gland
  3. Sublingual gland
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21
Q

Salivary glands

A

Units are called acini
Different types of cells producing enzymes and secretions
Produce large amount of saliva
Volume and amount of saliva under control of autonomic nervous system

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22
Q

Pancreas

A

Exocrine and endocrine functions

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23
Q

Exocrine functions of pancreas

A

Secretion of digestive enzymes and bicarbonate ions (HCO3) to the duodenum
Digestive enzymes break down nutrients
HCO3 neutralizes chyme

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24
Q

Endocrine functions of pancreas

A

Insulin and glucagon secretion

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25
Q

Liver

A

Storing and releasing nutrients that have been absorbed by the digestive tract
Produces and releases bile (fat digestion)

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26
Q

Gallbladder

A

Bile storage, concentrates, and pH changes, gets pushed down common bile duct to duodenum
Bile assists in fat digestion

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27
Q

Mucosa layer

A

Epithelium and lamina propria

Followed by submucosa

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28
Q

Submucosa

A

Contains many cells and glands that excrete into lumen

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29
Q

Muscular externa

A

Circular muscle contraction induces decrease in diameter of lumen
Longitudinal muscle contraction induces shortening of a segment of GI tract

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30
Q

Muscular muconsae

A

Innermost muscle layer that allows mucosa to fold and form ridges

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31
Q

Myenteric plexus

A

Outer nerve layer
Part of enteric nervous system
Between two muscle layers
Mainly controls motility of GI tract

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32
Q

Submucosal plexus

A

Inner nerve layer
Part of enteric nervous system
Located under mucosa
Control local secretion, absorption and submucosal muscle contraction
Receives sensory information from sensory neutrons in the GI tract

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33
Q

Epithelial cells in gut wall

A

Specialized in different parts of the GI tract for secretion or absorption, replaces al the time (every 5 days for total)
Includes secretory cells, endocrine cells and absorptive epithelial cells
Virtually all nutrients enter the body across the epithelium covering small intestinal villi

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34
Q

Central lacteal

A

Centre of villi, absorbs fat, lymphatic vessel, drains from intestine and rapidly flow into blood via thoracic duct

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35
Q

Splanchnic circulation

A

Blood supply to the intestine carries away absorbed water-soluble nutrients, flows to liver first via portal vein to be detoxified by hepatocytes

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36
Q

External anal sphincter

A

Under central control, skeletal muscle

there are two anal sphincters, internal anal sphincter is smooth muscle

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37
Q

Upper esophageal sphincter

A

Under central control, skeletal muscle

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38
Q

GI sphincters

A

Mainly smooth muscle, mainly positive resting pressure and regulate forwards and reverse movement

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39
Q

Enteric nervous system

A

Intrinsic innervation, mediated by nerve plexus in gut wall
Full length of GI system
Can and does function completely autonomously
Normal digestive function requires communicate between the intrinsic and CNS
100 million neurons (equal to spinal cord)

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40
Q

Extrinsic innervation

A

Autonomic nervous system, both parasympathetic and sympathetic systems

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41
Q

Sympathetic regulation

A

Inhibitory
Mainly postganglionic, connects directly to myenteric plexus (NE and rarely epinephrine), connects to submucosal for secretary processes, connects directly to epithelium
Pregangiolinc fibres arise from spinal cord (T5-L2) and terminate in pre vertebral ganglia (Ach)
Constant innervation

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42
Q

Sensory neurons

A

Monitor distension and inform enteric nervous system and brain

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43
Q

Stimulation of myenteric plexus

A

Increases tonic contraction of gut wall
Increased intensity and rate of contractions
Increased velocity of excretory waves along the gut causing more rapid peristaltic waves

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44
Q

Autonomic nervous system

A

Integrates activity of the enteric nervous system with the rest of the body
Do not directly innervate GI structure, but interact with ENS

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45
Q

Parasympathetic regulation

A

Excitatory
Mainly preganglionic and cholinergic, nerve fibres terminate on ganglion cells in enteric nerve plexuses and act on nicotinic ACH receptors
No direct innervation of the effector cells in gut wall
Vagal nerve fibres to basically all areas of the gut
Significant enervation in rectal column and anus via pelvic nerves

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46
Q

Afferent sensory nerve fibers

A

Strong afferent presence
Cell bodies either in ENS or dorsal root of ganglia in the spinal cord
Stimulated by irritation of the gut mucosa, distention of the gut, presence of chemical substances in the gut - sent to CNS
Activation can cause excitation or inhibition

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47
Q

Gastrocolic reflex

A

Reflexes from gut to pre vertebral sympathetic ganglia and back to GI tract
If you start eating when colon is full: signals from stomach to evacuate colon

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48
Q

Enterogastic reflex

A

Reflexes from gut to pre vertebral sympathetic ganglia and back to GI tract
Tells stomach that small intestine is still full, signals from colon and small intestine to inhibit stomach motility and secretion

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49
Q

Colonoileal reflex

A

Reflexes from gut to pre vertebral sympathetic ganglia and back to GI tract
Signals from colon to inhibit stomach motility and secretion

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50
Q

Vagovagal reflex

A

Reflexes from gut to spinal cord or brain stem and back to GI tract
From stomach and duodenum to the brain stem and back to control gastric motor and secretory activity

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51
Q

Pain reflex

A

Reflexes from gut to spinal cord or brain stem and back to GI tract
Cause general inhibition of the gut

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52
Q

Defecation reflexes

A

Travel from colon and rectum to spinal cord and back to produce powerful colonic, rectal and abdominal contractions required for defecation

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53
Q

Gastrointestinal peptides

A

Regulate the functions of the GI tract
Contraction and relaxation of smooth muscle and the sphincters
Secretion for enzymes for digestion (peptides acting on pancreas)
Trophic (growth) effect on tissues
Can regulate secretion of other GI peptides

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54
Q

Somatostatin

A

Inhibits secretion of all GI hormones

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55
Q

Acetylcholine

A

Neurocrine

Contraction of smooth muscle, relaxation of sphincters, increased salivary, gastric and pancreatic secretions

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56
Q

Norepinephrine

A

Neurocrine
Limited function under normal circumstances, relaxation of smooth muscle, contraction of sphincters, increased saliva secretion

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57
Q

Vasoactive intestinal peptide

A

Neurocrine

Inhibits smooth muscle contraction, stimulates secretion and vasodilation

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58
Q

Serotonin (5-HT)

A

Diverse motor and sensory function in GI tract, 90% serotonin in GI tract

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59
Q

Nitric oxide

A

Relaxes smooth muscle activity

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60
Q

Gastrin

A

Produces by G-cells in the antrum, released in blood circulation to act on parietal cells to release HCl in the stomach
Also has affect on mucosal growth

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61
Q

Cholecystokinin

A

CCK
Secreted by I-cells in the duodenum and jejunum, homologous to gastrin
Tries to inhibit gastric emptying
Stimulates gallbladder contraction and relaxation of sphincter of Oddi

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62
Q

Secretin

A

Secreted by S-cells in duodenum
Homologous with glucagon, stimuli for release is gastric juice entering into small intestine, leads to neutralization of acidity in the small intestine

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63
Q

Glucose-Dependent Insulinotropic Peptide

A

Secreted by K-cells in the duodenum and jejunum
Homologous to secretin and glucagon
Stimulates insulin release and gastric acid secretion (unlikely during normal physiological conditions)

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64
Q

Motilin

A

Biology not fully understood, in humans: 22 amino acid linear peptide
Released cyclically from gut in fasting state
Responsible for stimulating a specific pattern of GI motility: migrating motor complex

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65
Q

Ghrelin

A

Mainly released from stomach and pancreas, a little along complete gut
Stimulates vagal afferents that triggers the release of signals in the solitary nucleus and hypothalamus that promote food intake (including orexin and neuropeptide Y)
Release normally suppressed by leptin

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66
Q

Leptin

A

Released from adipose tissue

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67
Q

Somatostatin

A

Secreted by D-cells in gastric mucosa
Acidity of astral region stimulates somatostatin release
Also released by neutrons in the enteric nervous system
Inhibits release of gastrin and histamine, inhibits gastric acid secretion from parietal cells

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68
Q

Histamine

A

Secreted from enterochromaffin cells in the stomach, acts on H2 receptors on parietal cells
With gastrin and Ach, stimulates acid secretion by the gastric parietal cells
Secreted from mucosal mast cells and has a role as an immune mediator

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69
Q

Peristalsis

A

Food moves forward along tract
Ring of contraction on oral side of bolus that moves towards the anus, as ring moves, muscle in front of food bolus relaxes
Completely enteric
Usual stimulus if distention of the gut
Chemical irritation of the gut and strong parasympathetic stimulation can also induce peristalsis

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70
Q

Mixing movements

A

Allow digestive enzymes to come in contact with chyme and for chyme to come in contact with intestinal walls
Segments of contraction
Similar to peristalsis but no net movement

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71
Q

Single-unit types smooth muscle

A

Depolarization of area spreads via gap junctions to result in well coordinated contraction: ring of smooth muscle

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72
Q

Slow waves

A

Cyclic variations in GI smooth muscle resting potential
Typical in each part of the gut (3/min stomach, 12/min in duodenum)
Depolarizing phase caused by calcium influx and depolarization by potassium efflux
Maximal frequency that muscle contractions can happen

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73
Q

Threshold for contraction

A

Slow waves above this threshold cause contraction

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74
Q

Electrical threshold

A

Cause action potentials, contractions become bigger as action potentials increase

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75
Q

Slow wave amplitude

A

Increases with parasympathetic stimulation

Decreases with sympathetic stimulation

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76
Q

Baseline tension

A

GI muscle does not relax completely, tonically contracted

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77
Q

Interstitial cells

A

Pacemaker activity and decide when contractions occur
Transfer signals from enteric motor nerves to muscle cells
Set smooth muscle membrane potential
Responsible for generating slow waves, peristalsis and segmentation

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78
Q

Mastication

A

Chewing
Both involuntary and voluntary reflexes are involved
Food in mouth activates mechanoreceptors which coordinate reflex activity
Breaks down and lubricates food, mixes it with salivary enzymes
Important in breaking down cellulose membrane of fruit and vegetables

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79
Q

Bolus

A

Moist, chopped up food

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80
Q

Oral phase (swallowing)

A

Voluntary

Tip of tongue pushes food towards pharynx

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81
Q

Pharyngeal phase (swallowing)

A

Involuntary control
Series of protective reflexes initiated by the stimulation of afferent fibres in the pharynx and organized in the swallowing centre
Close off nasal, oral and laryngeal cavities
Respiration in inhibited

82
Q

Swallowing centre

A

Medulla and lower pons

83
Q

Esophageal phase (swallowing)

A

Food enters esophagus and upper sphincter closes, primary peristaltic contract moves and pushes food bolus down, lower esophageal sphincter relaxes and food bolus enters the stomach
Second peristaltic contraction clears esophagus of remaining food

84
Q

Dysphagia

A

Difficulty in swallowing
Can result in abnormalities in any components of swallowing reflex or anatomical structures
Common, especially in elderly (stroke, ALS, Parkinsons)
Risk of malnutrition, aspiration, choking

85
Q

Achalasia

A

Failure to relax
LES does not relax and open
Problem with myenteric ganglion nerves

86
Q

GERD

A

Gastrointestinal reflux disease
Acid gastric contents reflux to the distal esophagus
Very common, severity varies
May result in inflammation, ulcers

87
Q

Orad region

A

Stomach

Main area of reception and storage

88
Q

Caudad region

A

Main region of propulsion in stomach

89
Q

Stomach muscles

A

Longitudinal, middle circular, inner oblique

Body and fundus are thin walled, antrum is thicker with more muscle

90
Q

Pyloric sphincter

A

End of antrum entering into duodenum, prevents bolus from entering duodenum, causes mixing of food

91
Q

Gastric contractions

A

Allow stomach to grind, crush and mix ingested food

Lower part of stomach contracts to propel liquid chyme into duodenum in spurts

92
Q

Retropulsion

A

Lower and body and antrum contracts and propels food bolus to fundus

93
Q

Gastric emptying

A

Takes about three hours, liquids empty more rapidly than solids (less than 1 mm diameter), isotonic liquids empty faster, nature of contents affect emptying

94
Q

Migrating Myoelectric Complex

A

Empties non digestible material during inter digestive period

95
Q

Gastoparesis

A

Disorder where gastric emptying is delayed without evidence of obstruction
Symptoms: early satiety, nausea, vomiting, bloating and upper abdominal discomfort
Causes: system disease affecting neuromuscular function, education, injury to vagus nerve

96
Q

Pyloric stenosis

A

Congenital condition usually present infancy
Pyloric muscle thickens and pylorus fails to relax after a meal, leading to regurgitation and vomiting
Infants develop malnutrition and dehydration
Cured by surgical myotomey: longitudinal incision to muscle surrounding pyloric region

97
Q

Segmented contractions

A

Small intestine muscle contraction
Squirt luminal contents bidirectionally
Contractions increase resistance to flow, and there are more contractions upstream causing overall aborad movement

98
Q

Aborad

A

Away from the stomach

99
Q

Peristaltic contractions

A

Entry of chyme into duodenum causes peristaltic wave: travels only a few centimetres before dying out
Intestinal contents are slowly mixed and chyme is steadily moved

100
Q

Ileocecal valve

A

Prevents back flow from colon to ileum
Ileocecal sphincter is normally constricted, but strong peristaltic activity immediately after a meal relaxes the sphincter

101
Q

Colon storage

A

Mainly in distal colon

102
Q

Sigmoidscopy

A

Colonoscopy to sigmoid colon

103
Q

Hautrations

A

Circular and longitudinal muscles of colon contract simultaneously to form haustra, move back and forth to move contents

104
Q

Mass movements

A

1-3 times a day, move colonic contents over long distances

Final mass movement propels faces to rectum where they are stored until defecation

105
Q

Defecation

A

Involved both reflexes and voluntary actions
Upper portion of rectum relaxes to permit entry of faces
Rectal distention relaxes the internal anal sphincter
External sphincter is contracted until it is convenient to defecate (then voluntary)
Smooth muscle of rectum contracts and faces are forced out of body

106
Q

Hirschsprung’s Disease

A

Congenital megacolon, developmental abnormality where the ENS fails to develop
Segment of internal anal sphincter and upwards remains permanently contracted causing obstruction
Symptoms can be completely alleviated by surgical excision of diseased segment

107
Q

Irritable Bowel Syndrome

A

Motility disorder caused by visceral hypersensitivity, very common (10-30% of people)
Causes cramping, abdominal pain, bloating, gas, diarrhea, constipation
Partially due to dysmotility (consistent motor abnormalities have not been seen)
Patients with diarrhea have shortened transit times though intestines and increase in propulsive contractions in the colon
Patients with constipation-predominant disorders have slowed transit of intestinal contents

108
Q

Vomiting

A

Always centrally controlled, many triggers
Usually good to vomit
1. Hypersalivation
2. Fundus becomes flaccid
3. Sold palate rises, glottis closes, larynx moves forward, esophagus dilates, LES relaxes and moves upward
4. Diaphragm contracts, abdominal muscle contracts, gastric contents forced upwards

109
Q

Vomit control centre

A

Vomiting centre and nuclease tracts solitaires

110
Q

Parotid glands

A

Big, by ear

Serous glands

111
Q

Submandibular glands

A

Close to jaw bone
Mixed mucous and serous glands
Serous acinar cells secrete salivary amylase
Mucous cells secrete mucins
Intercalated duct drains into salivary duct which has striated and excretory ducts

112
Q

Sublingual glands

A

Under bottom teeth

Mixed mucous and serous glands

113
Q

Buccal glands

A

Smaller glands present in oral cavity, only secrete mucous

114
Q

Serous acinar cells

A

Secrete salivary amylase

115
Q

Two state model of saliva secretion

A

Primary secretion

Secondary secretion

116
Q

Primary secretion

A

Nearly isotonic, levels of Na, K, Cl and HCO3 are similar to plasma

117
Q

Secondary secretion

A

Ductal cells reabsorb Na and Cl ions from the saliva and secrete K and HCO3 into the saliva
Water does not follow ions but remains so saliva becomes more watery

118
Q

Saliva composition

A

Function of flow rate, the faster the flow rate the less time there is for ductal cells to act: saliva is closer to isotonic
~1L/day, pH 6-7

119
Q

Parasympathetic regulation of saliva secretion

A

Autonomic nervous system
Messages from tongue and other parts of oral cavity, stimulated by taste and pressure
Otic ganglion stimulation increases Ach and stimulates parotid gland
Submandibular ganglion stimulation increases Ach and stimulates submandibular gland

120
Q

Sympathetic regulation of saliva

A

Changes composition of saliva but no affect on volume

121
Q

Xerostomia

A

Dry mouth
Several different conditions cause decreases saliva secretion
Sjorgrens syndrome, side effects of many drugs, secondary to head and neck radiation
Decreased pH in mouth leads to tooth decays and esophageal erosions
Difficulty swallowing

122
Q

Gastric secretions

A

Mixture of secretions of the surface epithelial cells, mucous neck cells and gastric glands
1.5-2L/day
Largest volume is contributed by parietal cells
pH 1-3.5

123
Q

Mucous cells

A

All parts of gastric mucosa

Secrete mucus that coats and lubricates the gastric surface and protects epithelium

124
Q

Parietal cells

A

Body of stomach

Secrete HCl and intrinsic factor

125
Q

Chief (peptic) cells

A
Body of stomach
Secrete pepsinogen (pepsin precursor)
126
Q

G-cells

A

Antrum of stomach

Secrete gastrin hormone

127
Q

Gastric oxyntic gland

A

Located on body of stomach

Contains: epithelial cells, mucous neck cells, parietal cells, and chief cells

128
Q

Gastric acid secretion

A
  1. H/K pumps H into lumen
  2. Cl ions flow via Cl ion channels into lumen
  3. HCO3 is absorbed into the blood stream in exchange for Cl
129
Q

Pepsinogen

A

Inactive precursor of pepsin
Secreted by chief cells
Vagovagal reflex and gastrin release stimulates acid and pepsinogen release

130
Q

Intrinsic factor

A

Secreted by gastric parietal cells
Essential for absorption of vitamin B12 in the ileum
Secretion is only gastric function that is essential for human life

131
Q

Vitamin B12

A

Cobalamin
Involved in synthesis of all cells, affects DNA synthesis
Couples with R protein in small intestine, and breaks down from component R in alkaline conditions and binds to intrinsic factor
Absorbed when complex interacts with receptors in final parts of small intestine

132
Q

Pernicious anemia

A

Red blood cells fail to mature because of problem in intrinsic factor production and B12 absorption

133
Q

Regulating HCl secretion

A

Vagus nerves stimulate G-cells to release gastrin and parietal cells to release HCl
Distension on the antrum stimulates G cells to release gastrin

134
Q

Ulcer disease

A

Breaks in the stomach or in the duodenal mucosa
Corrosive action of pepsin and HCl on supper gastrointestinal tract mucosa
Caused be excess secretion of acid and pepsin by mucosa or diminished protective abilities of gastric mucosal barrier: Helicobacter pylori, non steroidal anti-inflammatories, alcohol, smoking, gastrinoma

135
Q

Gastric ulcers

A

Breaks in the stomach mucosa

136
Q

Duodenal ulcers

A

Breaks in the duodenal mucosa

137
Q

Helicobacter pylori

A

Bacteria that colonizes in the gut

Main cause for ulcers

138
Q

Gastrinoma

A

Zollinger-Ellison Syndrome

Rare tumour that releases gastrin hormone leading to excess HCl secretion

139
Q

Ductal cells

A

In pancreas
Secrete bicarbonate
Stimulated by secretin, CCK and Ach

140
Q

Aqueous component of pancreatic secretion

A

High bicarbonate concentration that neutralizes chyme in duodenum
pH ~8, isotonic with plasm
About 1L/day

141
Q

Enzyme components of pancreatic secretion

A

Proteases - proteins
Amylases - carbohydrates
Lipases - lipids

142
Q

Anicar cells in pancreas

A

Secrete enzyme components

Stimulated by CCK and Ach

143
Q

Pancreatic secretion and flow rate

A

Na remains constant
Bicarbonate increases with flow rate
Cl decreases with flow rate

144
Q

Pancreatic insufficiency

A

Rare
Secretion can drop down to 10% of normal without an effect on nutrient absorption: pancreatic enzymes are secreted in excess

145
Q

Pancreatitis

A

Inflammation of the pancreas
Auto digestion of pancreatic tissue due to enzyme retention
Can be caused by gallstones in ducts, malignancy, alcohol abuse
Medical emergency

146
Q

Cystic fibrosis

A

Pancreatic ducts are inefficient to secrete bicarbonate and water
Enzymes cannot be flushed properly from pancreas and limited quantities reach the intestinal lumen
Enzymes that reach lumen are inactive because of failure to neutralize gastric acid
Enzymes provided as supplements

147
Q

Bile

A
Secreted by liver continuously, 1L/day
pH 7.8-8.6
Isotonic
Flow into duodenum is intermittent
Diverted to gallbladder for concentration, acidification and increase in viscosity during inter digestive periods
148
Q

Bile acids

A

Synthesized from cholesterol in liver

In small intestine, bile salts that are more soluble

149
Q

Phospholipids (bile)

A

Lecithins: major

150
Q

Bile pigments

A

Bilrubin: major

151
Q

Sphincter of Oddi

A

Allows entry to duodenum from gallbladder
Closed while gallbladder is filled with bile
Relaxes shortly after eating (CCK induced gallbladder contraction)

152
Q

Primary bile acids

A

Chalice acid
Chenodeoxycholic acid
>90% of bile salts are reabsorbed from ileum not portal blood and resecreted by liver

153
Q

Secondary bile ducts

A

Deoxycholic acid
Lithocholic acid
Small amount of bile salts dehydroxylated by colonic bacteria, reabsorbed, returned to liver to be resecreted

154
Q

Gallstones

A

Collection of solid material, mainly cholesterol, in gallbladder
Often asymptomatic
Abdominal pain (upper middle, right), nausea, jaundice, fever

155
Q

Hyper secretion of cholesterol

A

Caused by obesity, oral use of contraceptives, estrogen, old age, sudden weight loss and genetic factors

156
Q

Diminished bile acid pool

A

Enterohepatic circulation is interrupted

157
Q

Cholecystectomy

A

Gallbladder removal
Gallbladder is not essential for normal digestive function: removal has no effect on life expectancy or metabolic status
Balance of specific bile acids may change, but no change on cholesterol
Inability to form concentrated bile and to secrete in coordinated fashion: patients have a harder time tolerating large fatty meals
Can have diarrhea

158
Q

Crohn’s disease

A

Inflammation that affects the full thickness of the bowel wall
Early onset, usually teens to early twenties
Abdominal cramps, diarrhea, weight loss, fever, anemia, ulcers, fistulae, abscess
Abnormal immune response to intestinal bacteria, mutations in NOD2 gene
No cure, but symptoms can be alleviated using medication, surgery, dietary adjustments ileal resection

159
Q

Ileal resection

A

40% resection is tolerated well
More causes bile salts to not be recirculated but secreted in diarrhea: causes depletion of bile salt, and fat absorption is impaired, also affects absorption of some vitamins, iron and calcium

160
Q

Transcellular route (epithelial cells)

A

Through epithelial cells from lumen to blood circulation

Large molecules only go via transcellular route

161
Q

Paracellular route

A

Between tight junctions

162
Q

Apical membrane

163
Q

Basolateral membrane

164
Q

Sucrose

A

Cane sugar
Disaccharide
Glucose + fructose

165
Q

Lactose

A

Milk sugar
Disaccharide
Glucose + galactose

166
Q

Starches

A

Large polysaccharides present in almost all non-animal foods

167
Q

Glycogen

A

Small amounts

Animal polysaccharides

168
Q

Cellulose

A

Large amount

Cannot digested and contributes to dietary fiber

169
Q

Amylase

A

Salivary and pancreatic alpha-amylases partially break down glucose polymers (alpha 1,4 bonds of amylose and amylopectin)
Not necessary for healthy humans, important in infants and pancreatic insufficiency
Inactivated by acidic pH in stomach

170
Q

Isomaltase

A

Only enzyme that an break down alpha 1,6 bonds of alpha-limit dextrins

171
Q

Sucrase-isomaltase

A

Brush border enzyme that binds sucrose

172
Q

Lactase

A

Brush border enzyme
Especially important in infants
If it is lacking, milk sugar does not break down and causes diarrhea

173
Q

GLUT5

A

Fructose transporter
Fructose is not natural product from corn
Excess amount can overwhelm transporter
Apical membrane

174
Q

SGLT1

A

Na-glucose transporter
Active transport
Apical membrane

175
Q

GLUT2

A

Transports glucose, galactose, fructose over basolateral membrane
Facilitated diffusion

176
Q

Essential amino acids

A

Many need to be obtained from dietary sources

177
Q

Pepsins

A

Inactive in the duodenum (pH >5)
Max, pepsin digests 15% of dietary proteins to small peptides and amino acids
Not necessary for protein digestion

178
Q

Enteropeptidase

A

Absolutely necessary to activate trypsinogen to trypsin and activate other pancreatic enzymes

179
Q

PEPT1

A

Absorbs peptides with a proton

Apical membrane

180
Q

Cytosolic proteases

A

Digests peptides absorbed into cells
Amino acids are secreted over basolateral side using transport proteins
Most are Na dependent

181
Q

Vitamin A

A

Retinoid acid
Regulates gene transcription
Fat soluble

182
Q

Vitamin D

A

Important in Ca absorption
Supplements: Cholecalciferol, ergocalciferol
Fat soluble

183
Q

Vitamin E

A

Tocopherol
Important antioxidant
Fat soluble

184
Q

Vitamin K

A

Important in blood clotting

Fat soluble

185
Q

Gastric lipase

A
pH optimum of 4-5.5
Resistant to pepsin
Hydrolyzes fatty acid linked to first position of triglyceride
Does not fully break down triglyceride
Inhibited by bile acids
186
Q

Pancreatic lipase

A

Acts on 1 and 3 positions of glycerol molecule to liberate esterified fatty acids
Neutral pH optimum
Inhibited by bile acids

187
Q

Lipase

A

Can absorb on the surface of fat droplet
Displaced by bile acids
Colipse binds both bile acids and lipase

188
Q

Phospholipase A2

A

Breaks down dietary phospholipids

189
Q

Cholesterol esterase

A

Degrades cholesterol esters derived form dietary sources and esters of vitamins A, D and E
Breaks down position 2 in triglycerides

190
Q

Emulsifiation

A

Large fat aggregate is exposed to bile, and non polar portions of bile salts and lecithin intercalate into the lipid
Polar parts demain at the surface
Bile sat/lecithin coat makes fat droplets easily fragmentable causing increased surface area

191
Q

Micelles

A

Formed from lipids breakdown products and bile acids
Transport lipids to brush border
Not necessary for triglycerides or glycerol
Necessary for cholesterol, plant sterols and fat soluble vitamins

192
Q

Apolipoproteins

A

Synthesized in rough ER and glycosylated, then coated in lipid cores to form chylomicrons

193
Q

Chylomicrons

A

Secreted from basolateral side of enterocyte via exocytosis and enter central lacteal

194
Q

Vitamins

A

Act as cofactors for many metabolic reactions

Must be acquired from diet

195
Q

Vitamin B9

A

Folate

Absorbed by at least three different transport mechanisms

196
Q

Water-soluble vitamins

A

B1, B2, B6, C, biotin, nicotinic acid, pantothenic acid

Absorbed by sodium dependent cotransport

197
Q

Sodium-coupled nutrient transport in intestines

A

Glucose transport is coupled to Na transport

198
Q

Na absorption in colon

A

ENaC
No glucose absorption
K absorbed with lumen concentration is high, or secreted if lumen concentration is low

199
Q

NHE3 and DRA

A

Na/H exchanger and Cl/HCO3 exchanger transport NaCl into epithelial cells

200
Q

KCC1

A

Transports Cl out of epithelial cells

201
Q

CFTR

A

Cl exists epithelial cells via cystic fibrosis transmembrane regulators
Phosphorylated by PKA, which is activated by cAMP (Gs protein, VIP and PGE2)
HCO3 also exits, either coupled with Cl or by itself

202
Q

Cholera toxin

A

Activates Gs protein, which leads to cAMP increase, activating CFTR, Cl efflux and watery diarrhea