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Physiology 210 > Gastrointestinal Physiology > Flashcards

Gastrointestinal Physiology Flashcards

1
Q

Functions of GIT

A

digestion, absorption, excretion, host defense

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2
Q

Digestion

A

form absorbable molecules from food through GIT motility, pH changes, and biologic detergents and enzymes

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3
Q

Absorption

A

movement of digestive food from intestine into blood or lymphatic system

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4
Q

Excretion

A

non-absorbable components of food, bacteria, intestinal cells, and hydrophobic molecules, cholesterol, steroids are excreted out of body

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5
Q

Host defense

A

GIT forms a barrier with the outside environment and contains a highly developed immune system

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6
Q

Components of the GIT

A

mouth, pharynx, esophagus, stomach, small intestine (duodenum, jejunum, ileum), large intestine

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7
Q

3 accessory organs

A

pancreas, liver, gallbladder

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8
Q

Structure of the intestine

A
  • lumen is the inside of the tube
  • contains many folds to increase surface area
  • circular fold where inner surface folds in on itself
  • contains villi
  • below the surface is called a crypt or invagination
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9
Q

Layers of GIT

A

mucosa, submucosa, muscularis externa, serosal layer

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10
Q

Layers of the mucosa

A

epithelium, lamina propria, muscularis mucosa

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11
Q

Epithelium layer

A
  • apical surface - inside of the tube or lumen
  • basolateral surface - closest to the blood surface, away from tube
  • selective uptake of nutrients, electrolytes, water
  • prevent passage of harmful substances
  • surface area is amplified by villi and crypts
  • stem cells within the crypts divide and produce daughter cells which differentiate into variety of cells
  • replaced every 5 days
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12
Q

Paracellular pathway

A
  • chemicals move between cells across the cell junctions
  • limited by tight junctions
  • water and small ions diffuse through tight junctions
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13
Q

Transcellular pathway

A
  • cross the cell and require transport proteins
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14
Q

Lamina propria layer

A
  • includes everything above the muscle layer
  • connective tissue, blood vessels, nerve fibers, lymphatic vessels/lacteals, immune, inflammatory cells
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15
Q

Muscularis mucosa

A
  • thin layer of smooth muscle
  • not involved in GIT contraction and may function to move the villi
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16
Q

Submucosa

A
  • contains blood vessels, lymphatic vessels, connective vessels and SUBMUCOSAL NERVE PLEXUS
  • relays info to and away mucosa
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17
Q

Muscularis externa

A
  • circular muscle - fibers are orientated in circular pattern and contract an relax to open and close tube
  • myenteric nerve plexus - regulate the muscle function of the GIT
  • longitudinal muscle - lengthens and shortens to control the tube length
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18
Q

Serosa

A
  • connective tissue layer that incases the intestine and forms connections with intestine and abdominal wall
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19
Q

Blood is _____ oxygenated entering the GIT but ___ oxygen as it perfuses the intestine

A

highly; loses

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20
Q

Where is blood taken from the GIT before going back to heart

A

the liver via the portal vein

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21
Q

Portal circulation

A
  • carries blood from intestinal tract to the liver
  • blood is nutrient rich
  • liver removes harmful substances
  • processes nutrients
  • hepatic artery and hepatic portal vein mix blood supply that is nutrient rich and poorly oxygenated
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22
Q

Hepatic artery

A

contains fully oxygenated blood that perfuses the liver

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23
Q

Hepatic portal vein

A

carries blood to the liver that has already perfused the stomach, pancreas, SI, LI

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24
Q

Liver is perfused in

A

series
- perfused by blood that has already perfused another organ

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25
Q

Reflexes regulating GI processes

A
  1. distension of the GIT wall
  2. osmolarity of contents
  3. pH of contents
  4. concentrations of specific digestion contents
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26
Q

Reflexes are propagated by these receptors

A

mechanoreceptors, osmoreceptors, chemoreceptors

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27
Q

Intrinsic regulation of GI processes

A
  • to control motility and secretion
  • contained wholly within organ
  • occurs through nerve plexi located in GIT wall
  • enteric nervous system - controls activity of secretomotor neurons, BRAIN OF THE GUT, independent of CNS, involuntary functions
  • two nerve networks - myenteric plexus and submucosal plexus
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28
Q

Myenteric plexus

A
  • found between two muscle layers (circular muscle and longitudinal muscle) of muscularis externa
  • influencing and regulation smooth muscle
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29
Q

Submucosal plexus

A
  • found in the submucosa
  • influences secretion
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30
Q

Extrinsic regulation of GI processes

A
  • outside of GIT wall
  • ANS - sympathetic and parasympathetic
  • smell of food signals through brain to GIT by ANS
  • different emotional states influence appetite
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31
Q

Parasympathetic response

A
  • stimulates large volume of watery saliva
  • stimulates peristalsis
  • stimulates secretion
  • stimulates bile released from liver
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32
Q

Sympathetic response

A
  • stimulates small volume of thick saliva
  • inhibits peristalsis
  • inhibits secretion
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33
Q

Long reflex

A
  • extrinsic pathway
  • smell of food/emotional state –> stimulates CNS –> efferent autonomic neurons fire and interact with same nerve plexus –> stimulates smooth muscle to contract or a gland to secrete –> causes response in GIT
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34
Q

Short reflex

A
  • intrinsic pathway
  • eating a meal activates receptors in GIT wall –> stimulus from receptors feeds into nerve plexus –> stimulates smooth muscle to contract or gland to secrete –> causes response in GIT
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35
Q

4 types of chemical messenger regulation

A

endocrine, neurocrine, paracrine, autocrine

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36
Q

Endocrine regulation

A

hormone secreting gland cell releases a hormone across its basolateral surface into the blood
hormone enters the blood and travels to target cell

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37
Q

Neurocrine regulation

A

nerve cell produces an electrical signal resulting in the release of a neurotransmitter which travels across a synapse and acts on a post-synaptic target cell

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38
Q

Paracrine regulation

A

local cell releases a paracrine substance which diffuses through the interstitial fluid to act on target cells in close proximity to the site of paracrine substance relase
apical surface of cell in lumen of gland

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39
Q

Autocrine regulation

A

local cell releases a substance which acts on the cell that released it

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40
Q

Endocrine cells

A
  • product hormons
  • found in the epithelium of the stomach and small intestine
  • enteroendocrine cells release hormons which control GI functions
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40
Q

3 GI hormones

A

secretin, cholecystokinin (CCK), gastrin
- all peptide hormones
- participates in feedback control system

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41
Q

Intestinal motility

A
  • stimulated by contraction and relaxation of the two muscle layers in the outer portion of the GIT, contents move along tract
  • peristalsis - main driving force
  • circular muscle contracts on the oral side of a bolus of food (longitudinal layer relaxes)
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42
Q

Segmentation

A
  • mixing of food
  • contraction and relaxation of intestinal segments with little net movement toward large intestine
  • allows mixing of GIT contents with digestive enzymes
  • slows the transit time to allow absorption of nutrients and water
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43
Q

Pacemaker cells

A
  • cells in the GIT that are distributed smooth muscle cells
  • constantly under spontaneous depolarization-repolarization cycles called slow waves under any circumstance
  • slow waves give GIT basic electrical rhythm
  • propagated through circular and longitudinal muscle layers through gap junctions
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44
Q

an increase of action potentials fired ____ the force of contraction

A

increases

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45
Q

3 phases of neural and hormonal GIT control

A

cephalic phase, gastric phase, intestinal phase

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46
Q

Cephalic phase

A
  • initiated through stimulation of receptors in the head by sight, smell, taste, chewing of food and emotional state
  • regulated by parasympathetic fibers that activate neurons in the GIT nerve plexus
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47
Q

Gastric phase

A
  • receptors in the stomach are stimulated by distension, acidity, amino acids, peptides
  • responses of stimuli are mediated by short (gastrin hormone) and long (acetylcholine neuron) neural reflexes
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48
Q

Intestinal phase

A
  • receptors in the intestine are stimulated by distention, acidity, osmolarity, digestive products
  • mediated by short and long neural reflexes, and hormones secretin, CCK, and GIP
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49
Q

Regulation of food intake

A
  • hypothalamus
  • contains a feeding center in the lateral region - increases hunger
  • contains a satiety center in the ventromedial region - decreases hunger
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50
Q

Orexigenic factor

A
  • increase intake
  • neuropeptide Y –> neuropeptide in hypothalamus that stimulates hunger or appetite
  • ghrelin –> synthesized and released from endocrine cells in stomach during fasting, released into blood and travels to hypothalamus stimulating release of neuropeptide Y
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51
Q

Anorexigenic factors

A
  • decrease intake or cause loss of appetite
  • leptin –> produced by adipose or fat tissue
  • insulin –> produced by the pancreas
  • peptide YY –> released from the intestine
  • Melanocortin –> released from the hypothalamus
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52
Q

Lack of leptin results in

A
  • no appetite regulation
  • overeating
  • obesity
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53
Q

Regulation of water intake

A
  • hypothalamus
    1. increased plasma osmolarity
    2. decreased plasma volume
    3. dry mouth or throat stimulated thirst
    4. prevention of over-hydration
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54
Q
  1. increased plasma osmolarity
A
  • osmoreceptors
  • stimulated thirst and release of hormones called vasopressin or anti-diuretic hormone to conserve water in kidneys
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55
Q
  1. decreased plasma volume
A
  • large blood loss or diarrhea and vomiting can cause dehydration
  • arterial baroreceptors will alter sympathetic and parasympathetic to increase arterial pressure to kidneys
  • activate renin-angiotensin system to produce angiotensin II which effects hypothalamus
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56
Q
  1. prevention of over-hydration
A
  • person stops drinking well before water is absorbed by GIT
  • mediated by stimulus from mouth, throat, GIT
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57
Q

3 pairs of salivary glands

A
  • parotid
  • submandibular
  • sublingual
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58
Q

What is saliva made of?

A

hypotonic and slightly alkaline
- water
- electrolytes (K and bicarbonate)
- digestive enzymes (amylase and lipase)
- glycoproteins (mucin)
- antimicrobial factors (lysozyme and lactoferrin)

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59
Q

Functions of saliva

A
  • moistens and lubricates food to make it easier to swallow
  • initiates digestion with digestive enzymes
  • dissolves small amount of food to allow it to diffuse to taste buds
  • prevents microbial colonization
  • aids in speec
  • buffer to neutralize acid
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60
Q

3 cells that make up salivary gland

A
  • acinar cells - secrete the initial saliva
  • ductal cells - create the alkaline and hypotonic nature of saliva
  • myoepithelial cells - mix of smooth muscle and epithelial cells
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61
Q

Path of saliva through the ducts

A
  • saliva moves from the acinus to the striated duct
  • myoepithelial cells contract to constrict the acinus end of the ducts
  • move the components of saliva toward straited duct
  • ductal cells modify the initial saliva to hypotonic, alkaline state
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62
Q

Tight junctions

A
  • acinar cells are leaky and allow water and small ions through
  • ductal cells do not allow the passage of water through
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63
Q

Acinar cells

A
  • water
  • proteins are released by exocytosis
  • Cl, HCO3, K are secreted
  • Na, H2O follow via leaky tight junctions
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64
Q

Ductal cells

A
  • net loss of Na and Cl
  • addition of K and HCO3
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65
Q

Regulation of saliva production

A
  • no hormonal
  • regulated by parasympathetic and sympathetic pathways (both stimulate salivary secretion)
  • dominant pathway - parasympathetic
  • increased blood blow to salivary glands results in increased secretion of saliva
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66
Q

Parasympathetic pathway for salivary gland function

A
  • stimulated by smell, taste, pressure receptors in the mouth, and during nausea
  • inhibited by tiredness, fatigue, sleep, fear, dehydration
  • some drugs have dry mouth side effect
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67
Q

Sympathetic pathways for salivary gland function

A
  • minor compared to parasympathetic
  • increases saliva flow
  • increases protein secretion from the acinar cells and stimulate myoepithelial cells to contract to increase flow
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68
Q

Amylase

A
  • found in saliva
  • enzyme that breaks down starches
  • also called ptyalin
  • inhibited by stomach acid
  • 95% of carbs digested in small intestine by pancreatic amylase
  • can only cleave alpha-1,4 linkages
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69
Q

Amylose

A
  • straight chain of glucose with alpha-1,4 linkages
  • breakdown leads to formation of maltose and matotriose
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70
Q

Amylopectin

A
  • chain of glucose with alpha-1,4 linkages and alpha-1,6 linkages
  • breakdown leads to formation of maltose, matotriose and alpha-limit dextrin
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71
Q

Lingual lipase

A
  • found in saliva
  • stable in acid, active in stomach
  • breaks down lipids
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72
Q

Conditions where salivary secretion is impaired / dry mouth

A
  • hereditary
  • sjogrens syndrome - immune system destroys salivary glands
  • side effects of drugs
  • radiation treatment
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73
Q

Consequences of dry mouth - xerostomia

A
  • dry mouth
  • decreased oral pH
  • difficulty in lubricating and swallowing food
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74
Q

Treatment for xerostomia / dry mouth

A
  • frequent sips of water
  • fluoride treatment to combat microbial populations
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75
Q

What initiates swallowing

A
  • pressure receptors in wall of pharynx
  • stimulated by food or liquid entering the pharynx and send signals to swallowing center in the brainstem
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76
Q

Steps of swallowing

A
  • chew food
  • tongue pushes it to the back of throat
  • soft palette elevates to stop food from entering nose
  • impulses from swallowing center inhibit respiration, raise larynx, and close the glottis
  • epiglottis covers the trachea to prevent fluid or liquid from entering the trachea
  • food descends into esophagus
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77
Q

Structure of the espohagus

A
  • top 1/3 is skeletal muscle and bottom 2/3 is smooth muscle
  • no absorption
  • mucus is secreted to lubricate food
  • stratified squamous epithelium (flat layers)
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78
Q

Structure of esophagus sphincters

A
  • upper esophageal sphincter just below pharynx - skeletal muscle
  • lower esophageal sphincter just below stomach - smooth muscle
  • both are closed except when swallowing, vomiting, burping
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79
Q

Main force of swallowing phase down the esophagus

A

peristalsis

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80
Q

Heart burn

A
  • lower esophageal prevents gastric contents from reaching esophagus (equal pressure of lower esophagus and stomach)
  • acid gets into esophagus and peristalsis pushes acid back down, increased salivary secretion
  • common when lower esophageal sphincter does not close properly, a big meal, pregnancy
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81
Q

Functions of the stomach

A
  • storage of food
  • mechanical breakdown of food
  • chemical breakdown of food - pepsinogen, HCl
  • reduces food to chyme
  • partial sterilization of food
  • controls rate food enters small intestine
  • secretes intrinsic factor important for absorbing vit B12
  • very little absorption - alcohol and little water
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82
Q

Stomach compartments

A

fondus and body
- upper part, thin smooth muscle
- mucus, pepsinogen, HCl are secreted
antrum
- lower part, thick smooth muscle, physical breakdown
- mucus, pepsinogen, gastrin are secreted

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83
Q

Pyloric sphincter

A

controls emptying of the stomach

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84
Q

Exocrine system

A
  • chemical messenger secreted into ducts and then onto an epithelial surface without passing into the blood
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85
Q

Major exocrine secretions in stomach

A
  • mucus - protects stomach epithelium from acid and digestive enzymes, helps to avoid self-digestion
  • HCl - hydrolysis of proteins into amino acids, dissolving food, digesting macromolecules, sterilization
  • pepsinogen - precursor to enzymes pepsin which is important for protein digestion
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86
Q

Mino secretions in stomach

A
  • intrinsic factor for vit B12 absorption
  • gastrin - endocrine - stimulates HCl
  • histamine - paracrine - stimulates HCl
  • somatostatin - paracrine - inhibits HCl
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87
Q

6 cell types in stomach

A

mucous cell, parietal cell, chief cell, enteroendocrine cell, ECL cell, D cell

88
Q

Mucous cell

A
  • luminal end of gland
  • produce mucus to protect stomach lining from cell digestion
89
Q

Parietal cell

A
  • secretes intrinsic factor and HCl
  • found in body and fundus
  • also known as oxyntic cell
  • modified surface with canaliculi (increase surface area)
  • as parietal cell activates, canaliculi becomes more defined
  • lots of mitochondria
90
Q

Chief cell

A
  • secretes pepsinogen (inactive precursor to pepsin - protein digestion, activated by acid)
  • found in all regions
91
Q

Enteroendocrine cell

A
  • secretes gastrin (+HCl and GI motility)
  • also known as G cell
  • found in antrum
92
Q

ECL cell

A
  • secretes histamine (+HCl)
  • found in all and antrum
93
Q

D cell

A
  • secretes somatostatin (-HCl)
  • found in all and antrum
94
Q
  1. Na+/K+ ATPase - acidification of stomach lumen
A
  • pumps 3 Na+ out and pumps 2 K+ in for every ATP
  • established electrochemical gradients with high K+ and low Na+ in cell
95
Q
  1. H+/K+ ATPase - acidification of stomach lumen
A
  • apical membrane of parietal cell
  • pumps out proton into lumen
  • active transport - ATP
  • as acid leaves, cell becomes more basic
96
Q
  1. carbonic anhydrase - acidification of stomach lumen
A
  • parietal cell gets rid of base by removing bicarbonate
  • H2O + CO2 = H2CO3
  • H2CO3 = H+ + HCO3-
97
Q
  1. Cl-/HCO3- exchanger - acidification of stomach lumen
A
  • bicarbonate is pumped out in exchange for chloride ion
  • secondary active transport
98
Q
  1. K+ channels - acidification of stomach lumen
A
  • K+ increase in cytosol and channels open to let K+ leave down its concentration gradient
  • diffusion through channels
  • loss of positive charge
99
Q
  1. Cl- channels - acidification of stomach lumen
A
  • apical membrane
  • Cl- lost into lumen of stomach diffuses through channels
  • compensates for loss of positive charge through K+ channels
100
Q

4 chemical messengers that regulate H+/K+ ATPase of parietal cell for stomach acidification

A
  1. gastrin - G cells, stimulates HCl
  2. acetylcholine - neurotransmitter, increased parasympathetic activity stimulates HCl
  3. histamine - ECL cells, stimulates HCl
  4. somatostatin - D cells, inhibits HCl, gastrin, histamine
101
Q

3 phases of gastric secretion

A

cephalic, gastric, intestinal phase

102
Q

Cephalic phase

A
  • stimulation in the brain
  • sight, smell, taste of food provides excitatory stimulation via vagus nerve
  • vagal nulcei in brain cause parasympathetic nerve to release acetylcholine at parietal cell to stimulate acid production
103
Q

Gastric phase

A
  • when food reaches stomach
  • causes G cells to release gastrin into blood
  • causes parietal cells to increase acid production
104
Q

Intestinal phase

A
  • when partially broken down food enters the duodenum
  • inhibitory phase due to presence of acid, fat, digestion products and hypertonic solutions
  • mediated by secretin and CCK
  • negative influence on gastrin production
105
Q

Indirect effects of ACh on acid secretion

A
  • stimulates ECL cells to release histamine
  • inhibits D cells to not release somatostatin
  • stimulates G cells to release gastrin
106
Q

Indirect effects of gastrin on acid secretion

A
  • stimulates ECL cells to release histamine
107
Q

What happens when acid secretion is occurring at high rates

A
  • ACh is released from parasympathetic nerves and will be reduced
  • H+ from parietal cells inhibit gastrin release from G cells
  • as ACh levels drop, somatostatin is not inhibited and has a direct effect on parietal cells and inhibits other chemical messengers
108
Q

Pyloric sphincter

A
  • sphincter between the antrum and duodenum
  • stronger force of contraction in the antrum will result in the sphincter closing
  • small amount of chyme enters the duodenum but there is backwards flow back into the stomach to allow for further mixing
109
Q

Causes of vomiting

A

psychogenic, gastrointestinal disturbances, inner ear infections, chemoreceptors in the brain and GI tract that can detect toxins, pressure in the CNS

110
Q

Vomiting center in the brain

A

medulla oblongata

111
Q

Body response to vomiting

A
  • nausea, salivation, breath held in mid-inspiration
  • glottis closes off trachea
  • lower esophageal sphincter and esophagus relaxes
  • diaphragm and abdominal muscles contract
  • reverse peristalsis moves upper intestinal contents into stomach
  • stomach contents move up through esophagus and out through mouth
112
Q

Benefits of vomiting

A
  • remove harmful substances before taken into body
  • nausea and feeling bad associated with vomiting are a negative conditioning, prevent from consuming noxious substance again
113
Q

Negative consequences of vomiting

A
  • dehydration
  • electrolyte imbalance
  • metabolic alkalosis - higher pH
  • acid erosion of tooth enamel
114
Q

What is a ulcer?

A
  • damage to or erosion of GIT mucosa
  • occurs in esophagus, stomach, or duodenum
115
Q

What causes an ulcer?

A
  • imbalance of aggressive factors (acid and pepsin) and protective factors (mucus and bicarbonate)
  • bacterial infection from Helicobacter pylori
  • NSADs, smoking, alcoholism, gastrinomas
116
Q

Treatment for ulcers

A
  • antibiotics to get rid of H. pylori infection
  • H+/K+ pump inhibitors
  • histamine receptor antagonists
  • prostaglandin-type drugs
117
Q

Gastric bypass surgery problems

A
  • no production of intrinsic factor - can’t absorb vit B12
  • higher amount of bacteria and no sterilization
  • no regulation of how much food enters the small intestine
118
Q

Exocrine pancreas

A
  • digestion
  • produces secretions that go into GIT
  • source of enzymes to digest carbs, proteins, fats, nucleic acids
  • secretes bicarbonate into duodenum to neutralize stomach acid (acid inactivates enzymes)
  • drain onto epithelial surface or apical surface
119
Q

Endocrine pancreas

A
  • producing hormones that regulate entire body
  • ductless gland
  • secretion occurs across basolateral surface for diffusion into blood
120
Q

Main pancreatic duct

A
  • drains exocrine secretions into small intestine
  • joins common bile duct from liver before entering
121
Q

Sphincter of Oddi / hepatopancreatic sphincter

A
  • common to bile duct and main pancreatic duct
  • regulates release of both contents into small intestine
122
Q

Pancreatic islets / Islets of Langerhans

A

produce the hormone insulin

123
Q

Pancreatic acinar cells

A
  • produce and secrete digestive enzymes
  • exocytosis of vesicles
124
Q

Pancreatic ductal cells

A
  • secrete bicarbonate for acid neutralization
  • secrete water
125
Q

Pancreatic juices

A
  • isotonic and alkaline
  • high in HCO3- and low in Cl-
  • Na+ and K+ same as in plasma
  • digestive enzyme
126
Q
  1. Cl- channel - HCO3- production of pancreatic cells
A
  • apical/luminal surface
  • CFTR channel allows diffusion of Cl- out of cell into lumen
127
Q
  1. Cl-/HCO3- exchanger - HCO3- production of pancreatic cells
A
  • Cl- in lumen is exchanged for HCO3- in cell
128
Q
  1. carbonic anhydrase - HCO3- production of pancreatic cells
A
  • catalyzes formation of H2CO3 from CO2 and water
  • H2CO3 dissociates into HCO3- and H+ and base is moved into duct lumen
129
Q
  1. H20 and Na - HCO3- production of pancreatic cells
A
  • water and Na+ follow paracellularly in response to electrochemical gradient
130
Q
  1. Na+/H+ exchanges - HCO3- production of pancreatic cells
A
  • secondary active transport
  • Na+ moving down its gradient provides energy to efflux H+ from the cell
131
Q

Alkaline tide

A
  • after a meal, acid is produced from parietal cell and enters stomach lumen
  • base leaves the cell into bloodstream as bicarbonate
132
Q

Acid tide

A
  • after a meal, base of produced from pancreatic duct cells and enters pancreatic lumen
  • acid leaves the cell into bloodstream at basolateral surface
133
Q

Pancreas function

A
  • source of major enzymes required for digesting carbohydrates, proteins, fats, and nucleic acid
  • starve without the pancreas
  • enzymes are packaged as proenzymes into zymogen granules that are stored in acinar cells
  • not activated until small intestine
134
Q

Enterokinase

A
  • in the apical/lumen surface of the epithelial cells of the duodenum
  • cleaves trypsinogen into trypsin
135
Q

Chymotrypsinogen

A
  • activated by trypsin to active enzyme chymotrpysin
136
Q

Pro-elastase

A
  • activated by trypsin to active enzyme elastase
137
Q

Pro-carboxypeptidase A and B

A
  • activated by trypsin to active enzyme carboxypeptidase A and B
138
Q

Lipase

A
  • hydrolyzes triglycerides into free fatty acids and monoglycerides
139
Q

Phospholipase A2

A
  • hydrolyzes phospholipids into free fatty acids and lysophospholipids
140
Q

Cholesterolesterase

A
  • hydrolyzes cholesterol-esters into free fatty acids and cholesterol
141
Q

Pancreatic S-cells

A
  • acid entering the duodenum from the stomach stimulates S-cells to produce hormone secretin (stimulates HCO3- release)
142
Q

Pancreatic I-cells

A
  • digested fat and protein entering the small intestine which stimulates CCK
  • CCK acts on acinar cells in pancreatic ducts to release digestive enzymes
143
Q

CCK negative feedback system

A
  • fatty acids and amino acids trigger CCK secretion into blood
  • CCK stimulates pancreas to release digestive enzymes and gallbladder to contract to release bile acids
  • as fats and amino acids are absorbed the stimuli for CCK is removed and stopped
144
Q

Pancreatic HCO3- negative feedback system

A
  • acid entering the duodenum from stomach stimulates secretin cells
  • secretin stimulates pancreas and liver duct cells to increase HCO3- secretion
  • stomach acid is neutralized and secretin stimulation is stopped
145
Q

Secretin and CCK inhibit

A

gastrin secretion

146
Q

Cystic fibrosis

A
  • Cl- channel involved in HCO3- secretion is mutated
  • patients produce all digestive enzymes
  • but HCO3- and water secretion is so minimal that enzymes don’t flush from ducts and do not reach intestine
  • pancreatic autodigestion and inflammation
  • patients need digestive enzymes supplements
147
Q

Gall bladder

A
  • small sac located underneath a lobule of the liver
148
Q

Steps of the liver and biliary ducts

A
  • bile duct runs from liver and join to form common hepatic duct
  • that joins with the common bile duct
  • main pancreatic duct and common bile duct join and release contents into duodenum
  • Sphincter of Oddi controls release into small intestine
149
Q

Liver systemic supply

A
  • arterial blood
  • hepatic artery contributes 25% of blood volume entering liver
  • blood is oxygen rich and nutrient poor
150
Q

Liver hepatic portal circulation supply

A
  • venous blood bring blood from stomach, spleen, pancreas, intestines
  • contributes 75% of blood volume
  • blood is oxygen poor and nutrient rich
151
Q

Hepatic lobule

A
  • functional unit of structure
  • hexagonal structure with central vein running through center and portal triad in each corner
152
Q

Portal triad

A

consists of hepatic artery, hepatic portal vein, and bile duct

153
Q

Hepatocytes

A
  • epithelial cells of liver
  • form tube like structures called canalicular networks
  • venous blood of hepatic portal system and arterial blood are mixed within hepatic sinusoids and flows slowly toward central vein
154
Q

Functions of the liver

A
  • exocrine gland
  • formation and secretion of bile
  • metabolizing and storing nutrients
  • deactivation and detoxification
  • producing circulating proteins
155
Q

6 components of bile

A
  • bile acids
  • cholesterol
  • salts
  • phospholipids
  • bile pigments
  • trace metals
156
Q

Emulsification

A
  • large lipid droplets need to be made smaller so pancreatic lipase can access them
  • mechanical disruption
  • emulsifying agents: amphipathic bile acids and phospholipids
157
Q

Micelle structure

A
  • polar head facing outside in contact with aqueous solution
  • non polar facing inside
  • single layer
  • soluble clusters of amphipathic molecules
158
Q

Micelle function

A
  • fatty acids and monoglycerides are very insoluble in water
  • a few diffuse into intestinal epithelial cells
  • majority are held in micelles which keep molecules in small soluble aggregates
  • equilibrium between free molecules and micelles
  • micelles are broken down and reformed
159
Q

Formation of bile

A
  • hepatocytes: produce and secrete bile acids
  • bile duct cells: add bicarbonate and other salts and water to bile
  • gallbladder: stores and concentrates bile between meals
160
Q

3 steps of bile acid recycling

A
  1. bile acids are released by the liver/gallbladder into duodenum for fat digestion
  2. bile acids are reabsorbed across the small intestine/ileum into portal circulation
  3. bile acids are transported back into hepatocytes
161
Q
  1. transport of bile acids from heptacyte into bile
A
  • move across apical surface of hepatocyte by primary active transport pathway into canalicular networks
  • canalicular networks drain into bile ducts and enter gallbladder or directly into small intestine
162
Q
  1. bile acids reabsorption from the ileum
A
  • digest food as moved through SI to ileum
  • move back to portal circulation by being absorbed through Na+ dependent secondary active transport pathway
  • bile acid then moved by facilitated transport across basolateral surface of enterocyte into portal blood
163
Q
  1. transport of bile acids from blood into hepatocyte
A
  • secondary active transporter into hepatocyte from portal blood so cycle can start over again
164
Q

Bile acids and cholesterol

A
  • bile acids are made of cholesterol
  • oatmeal and high fiber foods can bind to bile acids so they can be excreted in feces to reduce cholesterol
  • drugs and toxins can enter the hepatic circulation
165
Q

Regulation of hepatobiliary secretion by bile salts

A
  • as bile salts are absorbed from ileum and return to the liver, more will be secreted back into bile
166
Q

Regulation of hepatobiliary secretion by secretin

A
  • also controls bicarbonate production in the liver
  • produced and released by S-cells in duodenum
  • stimulated by acid in duodenum
167
Q

Regulation of hepatobiliary secretion by CCK

A
  • produced by I cells in duodenum and jejunum
  • stimulated by digested fat and proteins in SI
  • increases contraction of gallbladder and relaxes the sphincter of Oddi
168
Q

Gallstones

A
  • excess cholesterol
  • water insoluble and kept in micelles
  • if concentration of cholesterol becomes higher than bile acids, starts to precipitate
  • also requires a nucleating agent (protein, bacteria)
169
Q

Pigment stones

A
  • excess red blood cell breakdown, bile pigment increases
  • insoluble and concentrate in bile and form precipitates with calcium
170
Q

Gallstone treatment

A
  • cholecystectomy - gallbladder removal (low fat diet)
  • remove the stone
  • drugs to dissolve gallstones
171
Q

Function of duodenum

A
  • mixing of pancreatic digestive enzymes and bile with food
  • absorption of nutrients, iron, calcium
  • release of secretin and CCK
172
Q

Functions of jejunum

A
  • digestion and absorption
173
Q

Functions of ileum

A
  • digestion and absorption
  • absorption of bile acids and vit B12
174
Q

Stem cells can differentiate into 4 types in the small intestine

A

paneth cells, endocrine cells, goblet cells, enterocyte (absorptive) cells

175
Q

Absorptive cell (enterocyte)

A
  • has microvilli at apical surface (brush border membrane)
176
Q

Goblet cell

A
  • secretion of mucus for the lubrication of food and protection from acid
177
Q

Enteroendocrine cells

A
  • hormone producing cells into basolateral surface
  • I cells and S sells
178
Q

Paneth cells

A
  • secrete antibacterial peptides which protect the GIT from bacteria
179
Q

Intestinal absorption of glucose/galactose

A
  • intestinal lumen –> enterocyte through Na+ dependent glucose transporter (SGLT - secondary active transporter)
  • enterocyte –> basolateral blood through facilitated glucose transporter (GLUT)
180
Q

Intestinal absorption of fructose

A
  • intestinal lumen –> enterocyte through facilitated glucose transporter (GLUT5)
  • enterocyte –> basolateral blood through facilitated glucose transporter (GLUT2)
181
Q

Protein digestion in the stomach

A
  • pepsinogen is activated by stomach acid to pepsin
182
Q

Protein digestion in small intestine

A
  • pancreatic proteases - trypsin and chymotrypsin
183
Q

Further protein digestion in small intestine

A
  • carboxypeptidase - pancreatic protease
  • aminopeptidase - brush border enzyme
184
Q

Intestinal absorption of free amino acids

A
  • secondary active transport coupled to Na+
185
Q

Intestinal absorption of small peptides

A
  • secondary active transport coupled to H+
  • intracellular peptidases breakdown peptides into amino acids
186
Q

Absorption of amino acids

A
  • facilitated diffusion across the basolateral surface of enterocyte into circulation
187
Q

why are fatty acids and monoglycerides resynthesized into triglycerides as they pass through the epithelial cells?

A
  • maintain diffusion gradient from lumen of small intestine to epithelial cells
  • to allow triglycerides to be further processed for absorption
  • in the ER, triglycerides aggregate into lipid droplets that are coated with amphipathic proteins
  • droplets are then packaged into Golgi and secreted across basolateral surface
  • known as chylomicrons
188
Q

Where are chylomicrons absorbed?

A
  • by the lymphatic system by lacteals rather than capillaries because lacteals are leakier
  • lymphatics enter systemic circulation via thoracic duct
  • lipoprotein lipase found on endothelial cells of blood vessels break down triglycerides to monoglycerides and free fatty acids
189
Q

What form of iron is absorbed

A

divalent iron, Fe2+, ferrous iron

190
Q

Once inside intestinal, epithelial cells bind with protein:

A

ferritin
- acts as storage form of iron

191
Q

Absorbed iron that does not bind ferritin is:

A
  • released on blood side of enterocyte and transported in the blood attached to plasma protein transferrin
192
Q

When body stores of iron are high

A
  • production of ferritin is increased
  • increased binding of ferritin in epithelial cells
  • reduction in iron that is released into blood
193
Q

When body stores of iron are low

A
  • enterocytes produce less ferritin
  • less iron is retained in enterocyte
  • more will be absorbed into blood
194
Q

Iron toxicity

A
  • genetic defects in absorption control pathways
  • excessive iron supplementing in adult males or post-menopausal women
  • iron poisoning in children
195
Q

Iron deficiency

A
  • reduced number of size of red blood cells
  • tired, light-headed, headaches
  • not enough iron in diet, blood loss, menstruation, poor iron absorption, celiac disease, intestinal diseases
196
Q

What intestine absorbs more fluid?

A

small intestine

197
Q

Where does absorption and secretion occur in the small intestine?

A
  • fluid absorption at the villi
  • fluid secretion at the crypts
198
Q

Absorption of water in the small intestine

A
  • Na+/K+ ATPase generate a low intracellular Na+ concentration
  • creates a gradient for SGLT to move glucose and Na+ in the cell
  • Na+ gradient from low to high results in Cl- to follow the Na+
  • water follows those two gradients
199
Q

Secretion of water in the small intestine

A
  • NKCC1 transports Na+, K+, Cl- into cell
  • accumulation of Cl- in enterocyte
  • CFTR on brush border membrane open to allow Cl- to move out of cell
  • cAMP stimulates opening of CFTR
  • Na+ follow negative gradient of Cl-
  • water follows out of cell into lumen
200
Q

Migration myoelectric complex (MMC)

A
  • begins in lower portion of stomach and travels 2 feet along SI before dying out, next wave starts again at overlapping area
  • every 2 hours
  • push undigested material from the SI into the LI and prevent bacteria from remaining in the SI
201
Q

What regulated MMC

A
  • intestinal hormone motilin
  • initiates MMC
  • when you eat, motilin release is inhibited to allow the segmentation contractions to occur
202
Q

Lactose intolerance

A
  • lack of lactase enzyme from brush border to breakdown lactose into glucose and galactose
  • resulted in decreased water absorption in the gut (water is drawn into intestinal tract)
  • lactose containing fluid passes on to large intestine and bacteria digest lactose
  • causes gas, discomfort, diarrhea
203
Q

Cholera

A
  • consuming food or water contaminated with Vibrio cholera
  • vomiting and excessive diarrhea (20L a day)
  • dehydration, electrolyte imbalance, death
  • produces a toxin that increases cAMP production
  • Cl- channel stays open and lost into lumen and water follows
  • treat with clean water with salts and glucose to replace fluids
204
Q

Ileocecal valve

A
  • sphincter between cecum and ileum
  • open when ileum contracts after meal and closed LI is distended
  • retains LI contents
205
Q

Appendix/cecum

A
  • no apparent function in humans
206
Q

Ascending/transverse/descending/sigmoid colon

A
  • reabsorption of water (not as much as SI)
  • serve as reservoir for storage of waste and undigested materials prior to defecation
  • absorb products of bacterial metabolism
207
Q

Rectum

A
  • reservoir for feces
208
Q

Anus

A
  • two sphincters that control defecation
  • internal anal sphincter: smooth muscle/involuntary
  • external anal sphincter: skeletal muscle/voluntary
209
Q

Large intestine functions

A
  • only have crypts, no villi
  • smaller surface area
  • crypts have stem cells
210
Q

4 epithelial cells generated from stem cells in large intestine

A
  • absorptive cells (enterocytes): no brush border enzymes
  • lots of goblet cells
  • very little endocrine cells
  • very little Paneth cells
211
Q

Key function of large intestine

A
  • large ecosystem of bacteria
  • metabolize fiber into short chain fatty acids that are absorbed by diffusion
  • can produce vitamin (K) that are absorbed
  • produce gas
212
Q

Absorption of water in large intestine

A
  • similar to SI except no nutrient absorption (occurs in crypts)
  • no Na+ dependent nutrient channel, just a Na+ channel which allows Na+ into cell
  • Na+/K+ ATPase maintains gradient
  • Cl- follows positive charge of Na+
  • water follows chemicals
213
Q

Secretion of water in large intestine

A
  • identical to SI
  • NKCC1 transporter brings Na+, K+, Cl- into cell
  • Cl- increase inside cell, Cl- move out of cell down gradient
  • Na+ following negative charge of Cl-
  • water follows chemicals
214
Q

Mixing of the large intestine

A
  • segmentation in LI
  • slow basal electrical rhythm than SI to allow retention in the colon
215
Q

Propulsion of the large intestine

A
  • wave of intense contraction (mass movement) spread rapidly over large intestine pushing contents towards anus
  • occurs after eating to prior to defecation
216
Q

What’s in feces

A
  • water, undigested food, bacteria, epithelial cells
217
Q

Defecation reflex

A
  • rectum distends and activates mechanoreceptors
  • rectum contracts, internal anal sphincter relaxes and outer anal sphincter contracts
  • increased peristaltic activity in sigmoid colon, increasing pressure results in reflex relaxation of external anal sphincter
  • feces voided
218
Q

Toilet training

A
  • brain can override reflex relaxation of outer sphincter, delaying defecation to more acceptable time
  • delay results in reverse peristalsis and rectal contents moved back into sigmoidal colon
  • disadvantage of delay is more water absorption occurs and feces will be harder to void

Physiology 210 (12 decks)

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