Digestive System Flashcards

1
Q

What is the digestive tract?

A

A continuous tube from the mouth to the anus

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2
Q

Accessory Digestive Organs?

A
  1. Salivary Glands
  2. Pancreas
  3. Liver
  4. Gallbladder
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3
Q

Purpose of the GIT?

A

To break down food into small molecules which can be absorbed into the circulation

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4
Q

Six activities of GIT?

A
  1. Ingestion(chewing/swallowing)
  2. Secretion (chemical breakdown)
  3. Motility(Propulsion & Physical breakdown of food and secretions)
  4. Digestion
  5. Absorption(into bloodstream)
  6. Defacation(feces)
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5
Q

Homeostasis

A

Body activities are directed at maintain optimal and relatively constant internal conditions

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6
Q

How does the GIT help maintain homeostasis?

A

-Takes food and provides the body with nutrients it needs for growth/repair and function/regulation

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7
Q

What type of macromolecule does the GIT absorb most efficiently?

A

Carbohydrates(99% absorbed)

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8
Q

What type of macromolecules does the GIT absorb least efficiently?

A

Protein(92%)

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9
Q

T/F: The GIT has very efficient absorptive capacity?

A

True

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10
Q

What makes the GIT so efficient?

A

Propulsion, secretory activity and absorptive activities of the GIT are highly coordinated

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11
Q

What allows the GIT to be so coordinated?

A

It is innervated by neural and hormonal mechanisms

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12
Q

Describe the structure of the GIT?

A

-Tubular nature
- Opening at the mouth and anus

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13
Q

Why is the GIT considered an extracellular environment?

A

Since it is in contact with the external environment at both ends (mouth + anus)

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14
Q

Order of GIT structures?

A
  1. Mouth
  2. Stomach
  3. Small intestine
  4. Large intestine
  5. Anus
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15
Q

How long is the average GIT compared to a human?

A

Average height of a human is 1.5 meters and the average length of the GIT is 4.5 meters

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16
Q

How does the length of the GIT change in a cadaver?

A

-In cadaver the GIT can be up to 10 meters because there is no muscle contraction

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17
Q

What is the total surface area of the GIT?

A

In an adult it is between 200 to 250 m squared (which is 600x larger than the external surface area)

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18
Q

Why is the surface area of the GIT so large?

A

-Due to invaginations which allow the food to be in contact with the GIT for longer allowing it to be better absorbed/digested

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19
Q

Role of the salivary glands, liver, pancreas and gallbladder?

A

Put secretions into structures of the GIT

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20
Q

Four layers of the GIT(outside in)?

A
  1. Serosa
  2. Muscularis Externa
  3. Submucosa
  4. Mucosa
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21
Q

Where is striated muscles vs smooth muscle found in the GIT?

A

Striated Muscle : Found at the distal ends of the GIT(mouth to upper 1/3 of the esophagus + anus)
Smooth Muscle: Found in the medial portion of the GIT

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22
Q

What is the serosa?

A

Most external portion of the GIT it is a thin, tough layer of CT
-Continuous in places with the abdominal mesentery(holds the gut in place)

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23
Q

Two layers of the Muscularis Externa?

A
  1. Outer layer: Longitudinal fibers (decrease the length of the GIT)
  2. Inner layer: Circular fibers (decrease the diameter of the lumen)
    -Differ from striated to smooth depending where you are in the GIT
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24
Q

Submucosa?

A

-Loose CT containing lymphatics, blood vessels and neuronal network

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25
Q

3 Layers of the mucosa?

A
  1. Muscularis mucosa(smooth muscle)
  2. Lamina Propia(loose CT)
  3. Epithelial layer(in contact with food made up of secretory cells (exocrine + endocrine) & absorptive cells
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26
Q

T/F: The epithelial layer of the mucosa has invaginations to increase SA?

A

True

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27
Q

Regions of the GIT that are striated muscle?

A
  1. Oral cavity
  2. Parynx
  3. Upper 1/3 of the esophagus
  4. External anal sphincter
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28
Q

Neurons of the Enteric Nervous System?

A

Reside within the wall of the GIT

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29
Q

What is the Enteric Nervous System?

A

-Independent system that initiates, programs, regulates and coordinates activities of muscular, secretory & absorptive elements of the GIT

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30
Q

What is a Plexus?

A

Collection of nerve cell bodies

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31
Q

Where is the submucosal plexus found?

A

Between the muscularis mucosa and the circular muscle of the muscularis externa in the Gut wall

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32
Q

Where is the myenteric plexus found?

A

Between the circular muscle and longitudinal muscle of the muscular external in the Gut wall

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33
Q

What types of neurons are found in the two plexus?

A
  1. Sensory neurons
  2. Motor/Effector Neurons
  3. Interneurons
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34
Q

What do the sensory neurons do?

A

-Stretch receptors : sense stretch (ie. stomach is full)
-Chemoreceptors osmoreceptors: sense pH of the luminal content

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35
Q

What do Motor/Effector neurons do?

A

Activate the secretory and muscle cells

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36
Q

What do the interneurons do?

A

Expands the responses to stimuli in the GIT for integration over longer distances(increases the range of the ENS)
-Connect various neurons together

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37
Q

T/F: The ENS does not need the CNS to function?

A

True, all elements needed for the ENS are found in the gut wall

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38
Q

Excitatory Enteric Neuorns?

A

-Release acetylcholine(ACh) onto muscarinic receptors on muscle cells
-Result: increases contraction + secretion

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39
Q

What blockes Excitatory Enteric Neurons?

A

Atropine

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40
Q

Inhibitory Enteric Neurons?

A

-Non-adrenergic, Non-cholinergic transmitters, can release things like NO to decrease secretion and muscle contraction

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41
Q

Where do the neurons of the ENS synapse?

A

Onto smooth muscle cells, endocrine/exocrine cells and other ganglion cells

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42
Q

Cell bodies of the sensory fibers?

A

Cell bodies are in the plexuses and they get information from gut chemoreceptors & mechanoreceptors

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43
Q

Does the ANS synapse onto the muscles/glandular cells of the gut?

A

No, it synapses onto the enteric neurons

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44
Q

Parasymapathetic neurons?

A

Preganglionic(originate in the CNS and synapse onto the ENS)
-These synapse onto nicotinic receptors and release ACh causing an ecitatory response

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45
Q

Sympathetic neurons?

A

Postganglionic(extend from a ganglia and then onto the ENS)
-These synapse onto the enteric neurons via NA reeptors and release noradrenaline which causes an inhibitory response

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46
Q

Majority of the Parasympathetic input comes via?

A

The vagus nerve, at the distal part of the GIT input comes from the pelvic nerves

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47
Q

Majority of the sympatheic input comes via?

A

Sympathetic chain of ganglia

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48
Q

T/F: Parasympathetic and Sympathetic neurons can be both inhibitoey/excitatory?

A

True, when the sympathetic neurons synapse onto NANC neurons of the ENS they decrease inhibition but when sympathetic neurons synapse onto ACh neurons of the ENS they decrease excitation

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49
Q

How does the parasympathetic and sympathetic systems affect blood vessels?

A

Parasympathetic: Dilates blood vessels
Sympatheitc: Constricts blood vessels

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50
Q

ENS vs ANS reflexes?

A

ENS: Short intramural reflexes(within the gut wall)
ANS: Long extrinsic reflexes(outside of the gut wall)

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51
Q

Describe the two plexuses?

A

Anatomically distinct but behave as one functional unit

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52
Q

T/F : The parasympathetic /sympathetic system in the gut do the opposite in the CV?

A

True, in the gut the sympathetic system is inhibitory and in the CV the sympathetic system is excitatory

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53
Q

Sensory afferent fibers role?

A

-Sense the pH at the secretory cells and stretch in the GIT wall and sends the information to the CNS

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54
Q

Where do sensory afferent fibers send their information?

A
  1. Medulla: leads to the drive of the parasympathetic system on the gut
  2. Spinal cord: leads to the drive of the sympathetic system on the gut
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55
Q

Three ways that the CNS is activated to then activate the ANS?

A
  1. Afferent neurons(sensory fibers)
  2. Sight, smell, taste of food
  3. Emotional state
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56
Q

T/F: The ANS can allow for integrated activity over longer distances along the GIT?

A

True, for example the sight of food can cause you to salivate which can then result in an increase in stomach secretions to prepare for the food that is going to enter your stomach

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57
Q

Two types of hormones of the GIT?

A
  1. Non-GIT hormones: influence growth and development of GIT
  2. GIT hormones: may influence activity outside of the GIT but mainly regulate activities inside it
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58
Q

What type of GIT hormone is GHRELIN?

A

GIT hormone that influences activity outside of the GIT

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59
Q

How does GHRELIN work?

A
  1. During fasting, GHRELIN is released by glands in the stomach
  2. This leads to an incrase in appetite and stimulates hunger
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60
Q

How does LEPTIN work?

A
  1. Released by fat cells with overeating
  2. This leads to a decrease in appetite and induces satiety
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61
Q

Where do both GHRELIN and LEPTIN act?

A

Both hormones act on the hypothalmic feeding center to either increase/decrease appetite and satiety

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62
Q

What is meant by the diffuse endocrine system?

A

This is how hormones are diffused thorughout the GIT. They are not localized to one organ instead the hormones spread out throughout the mucosa

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63
Q

Largest and most diverse endocrine system in the body?

A

The Diffuse endocrine system of the GIT

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64
Q

Five most important GI hormones?

A
  1. Gastrin
  2. CCK
  3. Secretin
  4. GIP
  5. VIP
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65
Q

What is paracrine secretion?

A

When the hormone produced by the endocrine cell acts on another cell directly

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66
Q

What is autocrine hormonal regulation?

A

When the hormone produced by the endocrine cell acts on itself

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67
Q

What is endocrine secretion?

A

When the endocrine cell releases the hormone into the bloodstream and its effect acts at a distance on a target cell

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68
Q

GIT hormones are mostly ….

A

Peptides

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69
Q

How do GIT hormones reach their target cells?

A
  1. Hormone is released from the mucosa and into the portal blood via the hepatic portal vein
  2. The portal blood then travels through the liver and into the heart
  3. The blood then exist the heart and enters into the systemic circulation and where it binds to its target cells
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70
Q

GIT hormones target cells?

A

GIT hormones have multiple targets that can be either inhibitory of excitatory

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71
Q

How do GIT hormones interact with one another and with neurotransmitters?

A

Either synergistically or antagonistically

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72
Q

Define synergistically?

A

When two hormones work together and increase each others effects

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73
Q

Define antagonistically?

A

When two hormones act against each other and inhibit one another

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74
Q

What is propulsion in the GIT?

A

The flow of food through the GIT

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75
Q

Two factors affecting the flow of food through the GIT?

A
  1. Gradients of pressure (delta P)
  2. Resistance (1/R)
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76
Q

What is the main drive of flow in the GIT?

A

Coordinated contractions of muscular elements in the GIT wall

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77
Q

Segmentation?

A

-Circular muscle contraction(decrease lumen size)
-Effective movement of mixing

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78
Q

Peristalsis?

A

-Circular muscle contraction
-Wave of contraction moving over the wall of an organ, narrowing the lumen and setting up a gradient of pressure favouring aboral movement
-Effective at moving the contents forward

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79
Q

What place a more important role in the flow of food in the GIT the pressure gradient or the resistance?

A

The pressure gradient which is created by the muscle contractions

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80
Q

Why does resistance not really matter in the GIT?

A

There is normally little/no resistance in the GIT

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81
Q

T/F: Flow in through the GIT is aboral?

A

True, food typicallly flows away from the mouth

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82
Q

T/F: Flow in the GIT is slow?

A

True, flow must be slow so that food is properly broken down and absrobed

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83
Q

Phases of deglutition?

A

Decribes the phases of swallowing
1. Oral phase
2. Pharyngeal
3. Esophageal
4. Gastric

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84
Q

Only phase of deglutition that is voluntary?

A

Oral phase(when the food is in the mouth)
you can choose whether to swallow or not

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85
Q

Describe the oral phase?

A

-Transports food from the mouth to the pharynx (anterior to posterior portion of mouth)
-Voluntary control

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86
Q

Bolus?

A

Masticated, insalivated, mass of food

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87
Q

What part of the brain controls the voluntary aspect of the oral phase?

A

Cortex - gives you the ability to initiate chewing and swallowing

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88
Q

What part of the brain controls the involuntary aspect of the oral phase?

A

Deglutition center of the Medulla - once the decision to swallow has been made involuntary movements(coordinated reflexes) are initiated by the medulla

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89
Q

What leads to the activation of the deglutition center in the medulla?

A

“stretch” in the pharynx leads to the activation of the deglutition reflex
-Pharyngeal stretch receptors

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90
Q

What is the pharynx?

A

Region where the respiratory and digestive tracks cross

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91
Q

Describe the pharyngeal phase ?

A
  1. Bolus in the pharynx causes stretch and activates stretch receptors
  2. Reflexes from the deglutition center cause the bolus to move downward
  3. As the bolus moves downward it pushes on the epiglottis which closes the glottis
  4. Larynx moves under the tongue
  5. UES relaxes and pharyngeal muscle contracts to push the bolus across the relaxed UES into the esophagus
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92
Q

Why does the glotis need to be closed when swallowing?

A

To make sure the bolus goes through the esophagus into the stomach rather than through the trachea an into the airway

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93
Q

Describe the vocal cords when you swallow?

A

Larynx moves upward and forward to fit under the base of the tongue (this is reflexive)

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94
Q

Four involuntary reflexes that occur in the pharyngeal phase?

A
  1. Passage to nose, mouth and trachea are blocked
  2. Apnea
  3. UES relaxes
  4. Pharnyx muscles contract
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95
Q

What happens if UES does not relax?

A

Food won’t pass into the esophagus and will be stuck in the pharynx

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96
Q

T/F: the pharyngeal phase is under total involuntary control?

A

True

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97
Q

Deglutition Reflexes in the pharynx?

A

Initiated by the stimulation of afferent fibers in the pharynx
-Organized in deglutition centre
-Close off nasal, oral and laryngeal acitivity
-Prevent misidirection of the bolus
-Respiration is briefly inhibited

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98
Q

Describe the UES in the absence of a meal?

A

-Closed
- Impulses mediated by the vagal somatic nerve are tonically releasing ACh onto the striated muscle of the UES, causing it to remain contracted

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99
Q

Describe the UES during deglutition?

A

-Open
-Impulses from the vagal somatic nerve stop and this results in the relaxation of the striated muscle of the UES

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100
Q

The pharyngeal phase is stereotyped?

A

-Everything must occur in the same sequence everytime

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101
Q

Is the pharyngeal phase rapid?

A

-Yes, it takes about 1/5 of a second

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102
Q

Goal of the esophageal phase?

A

To move the bolus into the stomach via a peristoltic wave

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103
Q

Where is the esophagus ?

A

Within the thoracic cavity

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104
Q

Negative pressure of the thoracic cavity?

A

Has a negative pressure between -5 mmHg and -10mmHg

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105
Q

Pressure in the UES?

A

Pressure in the UES is very high because of the contracted muscles

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106
Q

Pressure in the LES?

A

Higher than the pressure in the esophagus

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107
Q

What would happen if the LES was always open?

A

Pressure in the LES would be lower than the intragastric pressure which. would cause gastric juices to flow into the esophagus and burn it

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108
Q

Intragastric pressure?

A

Slightly positive, lower than the LES due to its contraction

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109
Q

Two esophageal forces that push food forward?

A
  1. Gravity
  2. Peristalsis
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110
Q

Gravity as an esophageal force?

A

-Minor important; small effect for liquids and no effect on solids

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111
Q

Peristalsis as an esophageal force?

A

-Most important, wave of muscular activity to carry foods to the stomach

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112
Q

Primary Peristaltic Wave?

A

Each time we swallow a single primary peristaltic wave is generated
-Takes 8-10 seconds to propagate the length of the esophagus

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113
Q

Is primary peristalsis in the esophagus a deglutition reflex?

A

Yes, it is driven by the deglutition center in the medulla

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114
Q

Activation of primary peristalsis?

A
  1. Activation occurs goes from proximal to distal activation in the striated muscle of the upper 1/3 of the esophagus
  2. Activation occurs synchronously in the lower 2/3 of the esophagus in the smooth muscle
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115
Q

What activates the upper 1/3 of the esophagus?

A

Vagal motor neurons coming from the deglutition center and activate the wave sequentially

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116
Q

What activates the lower 2/3 of the esophagus ?

A

Some of the enteric neurons are activated by vagal autonomic, they are then able to relay and activate other enteric neurons (in an orderly fashion), this causes a contraction in the aboral direction, independent of the extrinsic nerves

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117
Q

Latency?

A

The time between the onset stimulation and the response

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118
Q

Integrity of the ENS is critical to the propagation of the peristaltic eave in the distal esophagus?

A

True, because in the proximal it iis dependent on the vagal motor neurons

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119
Q

What happens to peristalsis in the esophagus if you cut the Vagus nerve?

A

No more peristalsis

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120
Q

What happens to peristalsis if you cut the vagal nerves transthoracically?

A

-There will still be a primary peristaltic wave because the smooth muscle has the ENS necessary for the peristaltic wave

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121
Q

Vagus Nerve?

A

Essential for initiating peristalsis in the proximal esophagus

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122
Q

Intact ENS?

A

Essential for continuing and propagation peristalsis in the distal esophagus

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123
Q

Secondary Peristalsis?

A

Occurs when the bolus gets stuck in the esophagus

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124
Q

What happens when a bolus gets stuck in the esophagus?

A
  1. Causes local distension in the esophagus which the sensory afferent then sends this information to the deglutition center
  2. This then leads to enteric reflexes or long reflex
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125
Q

Enteric reflexes ?

A
  1. When the food gets stuck in the esophagus the esophageal distension triggers a local reflex response around the bolus which causes a secondary peristaltic wave to push the food further down
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126
Q

Long Reflexes?

A
  1. When food is stuck in the esophagus the esophageal distension causes vagal sensory inputs to the CNS
  2. These inputs cause more efferent vagal outputs which leads to a secondary peristaltic wave
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127
Q

Vagal-Vagal Reflex?

A

Sensory vagal afferents cause more output from vagal efferents

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128
Q

What is the LES and where is it located?

A
  • Terminal 4cm of the esophagus located 2 cm above the diaphragm and 2 cm below the diaphragm
    -Closed at rest
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129
Q

T/F: the LES shows a visible enlargement of circular muscle?

A

False

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130
Q

Closure of the LES at rest is…

A

Myogenic, LES tone is myogenically controlled

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131
Q

T/F: the LES has residual resistance in the absence of ENS or Autonomic innervation?

A

True

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132
Q

LES relaxation?

A
  • Neurogenic
    -Local ENS release of NANC (-) or vagal stimulation activates the inhibitory ENS neurons (parasympathetic system from the deglutition center activates inhibitory ENS neurons) decreases muscle tone
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133
Q

LES is a deglutition reflex ?

A

True

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134
Q

What happens when you bend you legs and increase intrabdominal pressure?

A

Intraabdominal pressure increase pressure equally on the stomach and the intraabdominal segment of the LES
ex. If abdominal pressure increases by 100 mmHg then so does the intrabdominal segment of the LES

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135
Q

Hiatus Hernia?

A

When the LES moved out of the diaphragm into the thorax

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136
Q

What happens in Hiatus Hernia when intraabdominal pressure increases?

A

An intraabdominal increase will not increase LES pressure now contents of the stomach will enter into the esophagus because now there is a pressure gradient from the stomach to the esophagus

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137
Q

Intrathoracic segment vs intraabdominal segment of the LES?

A

Intrathoracic segment : subject to negative pressure
Intraabdominal segment: subject to positive pressure

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138
Q

Anti-refluc mechanism?

A

Assisted by the presence of an intraabdominal segment of the LES

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139
Q

Heart burn?

A

burning sensation, radiating upwards in the chest towards the neck, due to acid reflux into the esophagus

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140
Q

Does Gastrin modulate the LES?

A

No, not at physiological levels

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141
Q

What hormones modulate the LES?

A

Progesterone, lowers the resistance in LES (ex. pregnancy you have increased progesterone and heart burn)

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142
Q

3 Motor functions of the Stomach?

A
  1. Temporary Storage
  2. Physical Disruption and Mixing of contents
  3. Propulsion into the duodenum
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143
Q

How much can the stomach store?

A

1-2 L

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144
Q

What is Chyme?

A

When the bolus is in a semi-liquid consistency

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145
Q

Four main regions of the stomach?

A
  1. Top: Fundus
  2. Body
  3. Bottom: Antrum
  4. Pylorus
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146
Q

Proximal vs Distal stomach?

A

Proximal
- Has thin wall of muscle meant for storing food for 1-2 hours
Distal
- Has a thick muscle eall meant for mixing & propulsion

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147
Q

Stomach wall structure(same as the GIT)?

A

-same four basic layers as the rest of the GIT (serose, musclaris external, submucosa, mucosa)

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148
Q

How is the Gastric mucosa different then the rest of the GIT?

A

-Consists of folds called Rugae
-Contains many different cell types
Arranged in pits/glands and all epithelial in origin

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149
Q

How is the muscularis externa different then the rest of the GIT?

A

-Contains an extra layer of smooth muscle (oblique muscle)

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150
Q

Empty stomach volume?

A

~ 50 mL
-intragastric pressure of +5 mmHg

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151
Q

How does the stomach accomodate a meal?

A

-Receptive Relaxation

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152
Q

What is receptive relaxation?

A

An increase in the volume of the stomach without significant increase in intraluminal pressure
-This is restricted to the proximal stomach

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153
Q

When does receptive relaxation occur?

A

Prior to the meals arrival in the stomach

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154
Q

How does receptive relaxation occur?

A

Deglutition centre sends vagal efferents which excite the inhibitory NANC (ENS) neurons which leads to the relaxation of musculature of the stomach

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155
Q

What happens when the meal is in the stomach?

A

The meal stretches the stomach and sends vagal afferents to the deglutition center which causes a vago-vagal reflexe that relaxes the stomach even more

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156
Q

What happens if the Vagi to the proximal stomach are cut?

A

-Receptive relaxation is limited, causing an increase in intragastric pressure which forces contents too quickly throug the stomach

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157
Q

What happens when the meal arrives to the stomach?

A

Further relaxation of the proximal stomach occurs due to local ENS inhibitory neurons releasing NANC neurotransmitter

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158
Q

Main form of contractile activity in the distal stomach?

A

Peristalsis, it starts in the middle of the stomach and then moves down to the sphincter

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159
Q

Is there peristalsis in the proximal stomach?

A

No, it is for storing the food

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160
Q

Peristalsis in the distal stomach results from?

A

-Local enteric reflexes in response to local distension

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161
Q

What determines the amplitude of the contraction(how strong the muscle contracts)?

A

Magnitude of the stimulus
ex. Amount of stretch and ACh on muscles

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162
Q

What determines the Frequency Direction velocity?

A

The electrical characteristics of the smooth muscle

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163
Q

Resting potential of the upper stomach?

A
  • (-55 mV)
  • No peristalsis
    -Has a steady resting potential
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164
Q

Potential of the lower stomach?

A
  • Between -45 mV and -55 mV
  • Rhythmic waves of partial depolarization in the lower stomach
    -These do not cause APs/muscle contractions since they don’t pass the threshold
    -Referred to as the basic electrical rhythm(BER)
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165
Q

Basic Electrical Rhythm(BER)?

A
  • Ongoing wave of depolarization in the lower stomach
    -10-15 mV
    -Lasts 1-4 seconds
  • 3 depolarizations per minute(even when sleeping or when you don’t have any food)
    -Non neuronal, not ENS pacemakers
    -Propagated from cell to cell
    -Found in both longitudinal and circular muscle
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166
Q

BER occurs synchronously along the circumference of the stomach?

A

Yes

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167
Q

BER occurs with a delay more distally?

A

Yes futher down the stomach the more of a delay from the initial BER, same depolarizations but now shifted forward in time

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168
Q

BER does not cause muscle contraction?

A

True

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169
Q

Spikes/Second Electrical Signal?

A

-Occurs at the peak of BER depolarization and these are what cause muscle contraction to occur

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170
Q

Magnitude of the stimulus determines the number of spikes ?

A

More stretch = More ACh released = More Spikes = More contraction(larger amplitude)

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171
Q

Number of spikes determines?

A

The amplitude of the muscle contraction
More spikes = Larger Muscle contraction

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172
Q

Maximum frequency of muscle contraction is?

A

3 muscle contractions per minute
This occurs when the stomach is full
-All BER peaks will have spikes

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173
Q

Location of the interstitial cells of Cajal?

A

-Located between the smooth muscle layers and the enteric plexuses, entending in circumferential and longitudinal direction

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174
Q

Role of the Interstitial cells of Cajal?

A

-Function as pacemakers for the spontaneous BER of the GIT
-Communication between nerves and muscle
- Coordinating groups of muscle cells

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175
Q

Spikes characteristics?

A

-Ca2+ dependent
- Found in logitudinal and circular fibers
-Stimulus = stretch + ACh
-Cell-cell propagation via gap junctions

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176
Q

T/F: peristaltic activity requires integrity of the ENS?

A

True

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177
Q

Muscle in the distal stomach?

A

Muscle becomes thicker the further into the distal stomach you go, closer to pyloric region = thicker muscle, closer to body = thinner muscle

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178
Q

Describe the contraction as it propagates down the distal stomach?

A

Band of contraction becomes wider and the contractions become stronger as it approaches the pyloric sphincter

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179
Q

Antral Systole?

A

When the entire terminal portion of the stomach (antrum + pyloric region) contract synchronously to close the pyloric sphincter

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180
Q

Pyloric Sphincter open/closed?

A

-Open at reast
-Closed by antral peristalsis
-Very narrow lumen: behaves as a filter for things moving from the stomach to the duodenum

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181
Q

Retropulsive Flow

A

Peristaltic contractions push food towards the pyloric end of the stomach. Antral systole then occurs which opens the pyloric sphincter in this brief period when the pyloric sphincter is open some of the chyme gets through to the duodenum but the majority does not and is squirted back into the body of the stomach at high velocity
-This aids in mixing and disrupting the chyme

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182
Q

T/F: Liquids and Solids are emptied from the stomach by different mechanisms

A

True

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183
Q

Gastric emptying of liquids?

A
  1. Emptying occurs due to a pressure gradient between the proximal stomach and duodenum
  2. There is receptive relaxation and therefore the dela P is small (liquid will flow through the stomach slowly)
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184
Q

Are liquids affected by the pyloric sphincter?

A

No

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185
Q

Vagotomy ?

A

When one or more branches of the vagus nerves are cut

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186
Q

How does a vagotomy affect the proximal stomach compared to the distal?

A

Proximal : relaxation cannot occur therefore delta P will be large and liquid will flow faster into the lower stomach
Distal: Liquid emptying stays the same

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187
Q

Where is the meal stored in the proximal stomach?

A

The fundic resevoir

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188
Q

Antral Pump?

A

Distal stomach functions as an antral pump to empty solids

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189
Q

How much the stomach can pump depends on what?

A

Frequency (3 contractions per minute)
Stroke volume (chyme fluidity and amplitude of the contraction)

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190
Q

Factors controlling Antral Peristalsis?

A
  1. Stretch of the muscle
  2. Local ENS reflex
  3. Vago-vagal reflex (send afferent back which sends info about th amplitude of the contraction)
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191
Q

What happens to emptying of solids if you cut the vagi?

A

-No longer have an afferent sending info to the CNS and thus will no longer have a vagi-vagal reflex
- Now antral peristalsis will only be caused by ENS reflex which will cause the emptying of the stomach to be slow

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192
Q

T/F: factors in the duodenum slow the rate of gastric emptying/antral peristalsis

A

True

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193
Q

Secretin and antral peristalsis?

A

Release of Secretin can further inhibit stomach contraction and slow it down

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194
Q

How does the duodenum slow antral peristalsis/gastric emptying?

A

Signals of distension, pH < 3, osmolarity and chemical composition all signal to the duoedenum to inhibit peristalsis via the vagus nerve afferent(Vago-vagal reflex), local ENS reflex and activates the sympathetic system

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195
Q

What happens if you cut the vagi to the distal stomach?

A

Emptying of the stomach will be sluggish

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196
Q

Enterogastric Reflex ?

A

Duodenal factors reduce the rate of gastric emptying/antral peristalsis

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197
Q

What is vomiting?

A

The emptying of the contents of the upper GIT

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198
Q

What happens when you vomit?

A

The proximal stomach and above relaxes and the upper duodenum and distal stomach contract

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199
Q

What increases intrabdominal pressure when vomiting?

A

Diaphragm lower and abdominal muscles contract

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200
Q

Is there reverse peristalsis when you vomit?

A

No, the esophagus and the GIT is mainly passive/relaxed

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201
Q

What part of the brain controls vomiting?

A

The vomiting center in the midbrain

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202
Q

Afferent information leading to the vomiting center?

A
  • Pharyngeal stimulation(something at the back of the throat)
    -GIT or urogenital distension
    -Pain, cardiac ischemia
    -Biochemical disequilibrium
    -Vestibular signals
    -Psychogenic factors
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203
Q

How does imbalance between parasymapthetic and sympathetic activities affect vomiting?

A

They precede and accompany vomiting causing sweating, vasoconstriction, salivation, alternating bradycardia and tachycardia

204
Q

Efferents from the vomiting center result in…?

A
  • Nausea
    -Retching
    -Vomiting (relaxation of the upper GIT + spasm of pyloric antrum and duodenum and contraction of abdominal muscles and diaphragm)
205
Q

Where is the vomiting center ?

A

Within the blood-brain barrier (cannot be induced by factors in the bloodstream)

206
Q

Chemoreceptor Trigger Zone(CTZ)?

A

Distinct from the vomiting center, sits outside the blood brain barrier in the medulla

207
Q

What does the CTZ do?

A

Circulating emetic agents in the blood stream act on the CTZ which sends signals to the vomiting centre to induce vomiting

208
Q

Is the CTZ required for vomiting?

A

No, but the vomiting center is

209
Q

What happens if your CTZ is not intact?

A

-You can vomit in response to afferents onto the vomiting center but you cannot vomit in response to circulating emetic agents

210
Q

Three stages of vomiting?

A
  1. Nausea
  2. Retching
  3. Emesis
211
Q

What nausea?

A

Psychic experience

212
Q

What is retching?

A

Abrupt, uncoordinated respiratory movements with glottis closed(gagging)

213
Q

What is emesis?

A

Expulsion of contents of the upper GIT mainly from the stomach but sometimes from the duodenum

214
Q

Reversal of thoracic pressure during emesis?

A

Emesis results from the reversal of thoracic pressure from negative to positive, as the diaphragm is displaced upwards, forcing esophageal contents to be expelled through the mouth

215
Q

What happens when you vomit?

A

-Take a deep breath, glottis closes, abdominal muscles contract, exerting pressure on the gastric contents

216
Q

Small intestine vs large ?

A

Small is larger than the large intestine but has a smaller diameter

217
Q

Three regions of the small intestine?

A

-Duodenum
-Jejenum
-Illeum

218
Q

Function of the small intestine?

A

-Most digestion and ALL absorption of nutrients occurs in the small intestine

219
Q

Four functions of the upper small intestine?

A
  1. Neutralization
  2. Osmotic equilibrium
  3. Digestion
  4. Absorption
220
Q

Why does chyme need to be neutralized in the small intestine?

A

-Chyme from the stomach is highly acidic and must be rapidly neutralized because the small intestine mucosa is not as well protected as the stomach

221
Q

What is osmotic equilibrium in the small intestine?

A

Chyme entering the small intestine is hypertonic fluid is then added in the small intestine so that when it leaves it is isotonic

222
Q

Motor activities of the small intestine?

A

-Effective mixing
-Slow propulsion (2-6 hours)
Slow movement of contents forward to absorb/breakdown nutrients

223
Q

Frequency of intestinal contractions?

A

Determined by the BER which is at a higher frequency in the SI compared to the stomach

224
Q

Spikes of the intestinal contraction?

A

-Initiated by stretch or ACh

225
Q

Amplitude of the small intestine contractions?

A

-Related to the number of spikes/burst of ERA

226
Q

How does frequency of the BER change throughout the SI?

A

Frequency of the BER decrease systematically from the proximal to distal intestine
In the duodenum it is 12 BER/min at the illeum it is 8 BER/min

227
Q

Insterstitial cell of cajal in the intestine?

A

Drive the BER at different rates in the SI and each group of pacemakers drive about 1000 cells in the intestine

228
Q

Proximal intestine vs Distal small intestine?

A

Proximal
-f of BER is greater
-Excitability of smooth muscle is greater(don’t need as much ACh/stretch for a stronger contraction)
-Thickness of smooth muscle is greater
-Frequency + amplitude of muscle contractions are greater in the proximal small intestine

229
Q

Most common type of contractile activity in the SI after a meal?

A

Segmentation

230
Q

How is segmentation mainly controlled in the SI?

A

Myogenic response to distension
- When the muscle is stretched the circular muscles contract for effective mixing

231
Q

How does the ENS control segmentation in the SI?

A

Coordinates and organizes contraction over a length of SI

232
Q

How do Hormones and the ANS modulate segmentation in the SI?

A

Parasympathetic increases and sympathetic decreases

233
Q

How does segmentation ensure slow propulsion?

A

The contractions at the proximal end of the SI will be stronger and more frequent(higher resistance) whereas at the distal end they are slower and weaker(lower resistance) this creates a slow, net aboral propulsion

234
Q

Is there peristalsis in the SI?

A

yes, but it is infrequent, irregular, weak, shallow and travels for short distances only a few centimeteres

235
Q

When is Peristalsis seen in the SI?

A

During pathological conditions such as diarrhea which causes fast movement through the SI

236
Q

Intestinal Peristalsis?

A

-Mediated by a series of local reflexes
-Involves interaction of longitudinal and circular muscle
-Maximum f cannot exceed f of BER
-Requires integrity of the ENS
-Modulated by the ANS and hormones

237
Q

Law of the intestine?

A

-When the SI stretches the receptors this results in contraction of the logintudinal muscle and relaxation of the circular muscle AHEAD of the bolus and contraction of the circular muscle and relaxation of the logitudinal muscle behind the bolus(this is all neurally mediated)
-Both together result in the forward movement of the bolus

238
Q

Colon contractile activity?

A

-Similar to that in the SI but slower, more sluggish and irregular

239
Q

T/F: Digestion and absorption is completed in the SI?

240
Q

What can be absorbed in the colon?

A

H2O and some ions

241
Q

Functions of the colon?

A
  1. Mixing (promotes absorption of water + ions)
  2. Propulsion(slow(50-60 hours for conversion of chyme to feces))
  3. Storage(resevoir for chyme)
242
Q

How much chyme enters the colon per day and how much leaves?

A

1500mL/day enters and after the water and ions are absorbed 200mL/day leaves

243
Q

T/F: the illeocecal sphinter is normally closed?

244
Q

Where in the colon does mixing occur?

A

In the Ascending colon and transverse colon

245
Q

Where in the colon does propulsion and storage occur?

A

In the descending colon and the sigmoid colon

246
Q

BER in the colon?

A

The colon has an irregular BER that controls segmentation and peristalsis

247
Q

How many times does the large intestine empty its contents?

A

2-3x a day, corresponding to the intake of a new meal and increased activity in the colon and distal SI

248
Q

What reflexes are activated by the presence of a meal in the stomach?

A

Gastrocolic reflex and Gastroileal reflex

249
Q

Gastrocolic reflex?

A

Moves contents from the sigmoid colon to the rectum

250
Q

Gastroileal reflex?

A

Opening of the illeocecal sphincter which leads to the ileocolic reflex(increased acitivty at the distal ileum)

251
Q

Interdigestive period?

A

Time between meals when the small intestine and stomach are mostly empty

252
Q

What occurs during the interdigestive period?

A

GI motility is organized into an intense pattern of cyclic myoelectric(motor) acitivty)
-Occuring every 90 minutes at regular intervals
-Moving sequentially over the distal stomach and small intestine up to the distal illeum

253
Q

Migrating Myoelectric Motor Complex(MMC)?

A

What your distal stomach and small intestine do during the interdigestive period

254
Q

Phase I of the MMC?

A

Lasts 60 mins and there are no spikes or contractions

255
Q

Phase II of the MMC?

A

Lasts 20 mins and there are irregular spike potentials and some contractions

256
Q

Phase III of the MMC?

A

Lasts 10 mins and there are regular spike potentials and contractions

257
Q

How does the MMC travel through the SI?

A

Each segment of the SI undergoes the 90 min MMC cycle during the interdigestion period it gradually goes down the SI

258
Q

What does the MMC do to food?

A

Causes the forward propulsion of food with no retropulsive flow

259
Q

What is the MMC restricted to?

A

The distal stomach and the small intestine

260
Q

Does the CNS or ANS initiate MMC?

261
Q

What initiates the MMC?

262
Q

What propagates the MMC?

A

ENS with modulation via ANS and Gut peptides

263
Q

What stops the MMC?

A

Intake of a new meal

264
Q

Housekeeping function of the MMC?

A

Used to move things through the GIT that have not been able to move through because the MMC does not close the pyloric sphincter

265
Q

Gastric emptying of large, nondigestible partciles via MMC?

A

Large particles that were unable to go through the sphincter are now able to pass as well as cells that sloughed off and enzymes in the stomach that need to be removes

266
Q

Two types of secretion in the GIT?

A
  1. Exocrine
  2. ENdocrine
267
Q

Exocrine secretion vs Endocrine?

A

Exocrine:
- Secretions moved into the lumen of the GIT
Endocrine:
-Secretion into the bloodstream

268
Q

Why is exocrine considered external environment?

A

Since it is released into the lumen of the GIT which is in contact with the external environment at the mouth and anus

269
Q

Chemical Breakdown of food?

A

Occurs progressively as food is broken down into smaller molecules and results from the secretory activity of many exocrine glands found within and in association with the GIT

270
Q

Secretion is …..

A

An active, energy and blood flow-dependent process

271
Q

What is secretion?

A

The release of fluids containing ions and enzymes

272
Q

Three types of enzymes?

A
  1. Amylases
  2. Proteases
  3. Lipases
273
Q

What regulates secretion?

A

Near the proximal end of the GIT(mouth) secretion is neurally regulated
Near the distal end of the GIT(large intestine) secretion is hormonally regulated

274
Q

Three Salivary glands?

A
  1. Parotid
  2. Submandibular
  3. Sublingual
    Each secrete something different
275
Q

Mucin?

A

A type of secretion that protects and lubricates

276
Q

Salivary Amylase?

A

Begins carbohydrate digestion in the mouth and is active at neutral pH

277
Q

Lingual lipase?

A

Produced by the tongue for lipid digestion and is only active at acidic pH (not active till it reaches the stomach)

278
Q

What does the parotid gland secrete?

A

Serous fluid

279
Q

What does the sublingual gland release?

A

Mucin-rich fluid

280
Q

What does the submandibular gland release?

A

Mix of mucin rich and serous fluid

281
Q

How are the salivary glands fluid released into the mouth?

A

Via the ducts of salivary glands

282
Q

How much saliva do we produce per day?

A

0.5-1.5 litres per day

283
Q

Ions found inside the saliva?

A

Na+, K+, Cl-, HCO3-

284
Q

What types of secretion is saliva?

285
Q

pH of saliva?

A

Between 6.5 and 7.0

286
Q

What is Ptylin?

A

A form of amylase that opperates at neutral pH and breaks down carbohydrates

287
Q

Secretions found in saliva?

A

-Ptylin
-Lipase
-Lysozyme
-Mucin

288
Q

How are the salivary glands regulated?

A

Neurally via the ANS since they are proximal in the GIT

289
Q

Parasympathetic regulation of the salivary glands?

A

Sends excitatory efferents onto the ENS which release ACh and lead to an increase in secretion and vasodilation

290
Q

What prevents salivary gland secretion?

A

Atropine (blocks the musacarinic receptors)

291
Q

Does the sympathetic system affect the salivary glands regulation?

A

No, but if it did it would cause vasoconstriction

292
Q

Simple and conditioned reflexes that activate salivary glands?

A

-Seeing food, hearing food and smelling food and activating sensory receptors in the mouth (ex. sticking your finger in your mouth) causes the salivary centers in the medulla to send efferent via the parasympathetic systems to increase secretion from salivary glands

293
Q

Cephalic phases of secretion?

A

Psychic - conditioned reflex(smelling food/seeing food)
Gustatory - taste(having food in mouth)

294
Q

Other phases of secretion?

A

Gastric(food in stomach)
Intestinal (food in intestines)

295
Q

How much mixed gastric juice do we produce per day?

A

1.5 to 2.0 litres per day

296
Q

Composition of gastric juice?

A

Isotonic
-Na+, K+, Cl-, H+(high concentration to make acidic)

297
Q

pH of gastric juices?

298
Q

Secretions in the gastric juice?

A

-HCl
-Pepsinogen
-Intrinsic factor
-Mucin

299
Q

T/F: Protein digestion requires multiple enzymes and multiple steps/intermediates?

A

True(Protein becomes a smaller peptide and then individual amino acids and these steps require different enzymes)

300
Q

Tubular Glands of the cardiac and pyloric?

A

Secrete an alkaline and mucin-rich fluid

301
Q

Tubular Glands of the Fundus and Body?

A

Secrete acid, enzymes and intrinsic factor

302
Q

Why are tubular glands shaped like tubules?

A

To increase the surface area at the level of the stomach to allow for more digestion + breakdown

303
Q

Gastric cells in the Fundus and body?

A
  1. Parietal cells
  2. Chief cells
  3. Mucous neck cell
304
Q

Parietal Cell

A

-Secretes HCl
-Contains lots of mitochondria
- Has intracellular canaliculi at its apical surface to increase surface area

305
Q

Postprandial alkaline tide?

A

When a bicarbonate ion diffuses into the bloodstream to restore intraceullar pH this causes an increased alkalinity in the venous blood (increases pH)

306
Q

Parietal Cell pH?

307
Q

Does parietal cell secretion change depending on type and magnitude of stimulus?

308
Q

How does the pH of the gastric juice change?

A

The pH of the gastric juice depends on the number of parietal cells that are active (the more active = the lower the pH of the gastric juice)

309
Q

Functions of the HCl?

A
  1. Precipitates soluble proteins (proteins stay in the stomach longer)
  2. Denatures proteins(more readily digestible)
  3. Activates pepsin
  4. Provides optimal pH for pepsin
310
Q

What do the chief cells secrete?

A

Pepsinogen

311
Q

What cells release intrinsic factor?

A

Parietal cells

312
Q

What is the only secretion of the stomach that is essential to life?

A

Intrinsic factor

313
Q

What is intrinsic factor?

A

-A glycoprotein
-Required for absorption of Vitamin B12 in the distal small intestine(illeum)

314
Q

What happens if you lack intrinsic factor ?

A

Intrinsic factor can no longer complex with vitamin B12 which will now be broken down in the stomach and will lead to pernicious anemia

315
Q

Zymogen Granules?

A

Released by the parietal cells, these are pepsinogen that is in its inactive form

316
Q

How does pepsinogen become active?

A

In the presence of HCl pepsinogen is converted to its active form pepsin. Once some pepsin is available it will act on pepsinogen to activate even more(autocatalysis)

317
Q

Role of HCl form pepsinogen ?

A

-COnvert pepsinogen to pepsin
-Maintain acidic pH for proper pepsin function

318
Q

What does pepsin do?

A

Breaksdown proteins

319
Q

Locations of mucin secretion?

A

-All surface epithelial cells
-Cardiac and pyloric tubular glands
-Mucous neck cells(funds and corpus)

320
Q

Where is the Muci-Bicarb layer located?

A

Present in all parts of the GIT where mucous is secreted

321
Q

What is the Muci-Bicarb layer?

A

Surface epithelial cells produce mucin which produces a gel layer on top of the epithelium

322
Q

How does the Muci-bicarb layer protect the GIT from acid?

A

H+ ions can freely move into the Muci-bicarb layer but when they interact with the layer it will lead to them combining with HCO3- and producing CO2 and H2O

323
Q

How does HCO3- get into the Muci-bicarb layer?

A

Surface epithelial cells also secrete bicarbonate which becomes adsorbed through the mucous and gets stuck

324
Q

pH outside vs inside the Muci-Bicarb layer?

A

Outside the pH is 2 and inside it is 7

325
Q

Where is the gastric mucosal barrier located?

A

Only in the stomach

326
Q

What is the GMB and what is its function?

A

-Additional protection to prevent stomach damage
-Apical surfaces of the epithelial cells are held together by tight junctions

327
Q

Re-epitheliazation?

A

Cells in the gastric mucosa are constantly being recyled and replaced to ensure everything is protected and working properly

328
Q

Two causes of ulcers due to a weak barrier?

A

-Aspirin & NSAIDs(weaken the barrier)
-Helicobacter pylori

329
Q

How does helicobacter pylori weaken the barrier and contribute to ulcers?

A

it is a bacteria that can burrow into the top of the epithelia and release a toxin that can damage the GMB and lead to an ulcer

330
Q

Possible cause of excessive HCl output that could lead to ulcers?

A

Gastrin-producing tumours, will produce gastrin constantly stimulating the parietal cells to constantly release HCl

331
Q

Secretion in the stomach is regulated by?

A

Both neural and hormal control

332
Q

Hormones that regulate stomach secretion?

A

-Gastrin
-Histamine
-Somatostatin

333
Q

Three phases of Gastric secretion?

A
  1. Cephalic(psychic + gustatory)
  2. Gastric
  3. Intestinal
334
Q

Neural regulation of secretion?

A

Parasympathetic efferents synapse onto ENS which activate excitatory enteric neurons that release ACh onto secretory cells this depolarizes the cell and granules containing the enzymes get released

335
Q

What cells can neural regulation of secretion activate?

A
  • Parietal (releases HCl)
    -Peptic (releases pepsin)
    -Mucous(releases mucin)
336
Q

How is the cephalic phase mediated?

A

Via vago-vagal inputs from the parasympathetic system

337
Q

T/F: Secretion leads to vasodilation?

338
Q

How does the sympathetic system affect gastric secretion?

A

-Inhibits secretion and leads to vasoconstriction
-Sympathetic system is inhibited due to stretch

339
Q

Gastric phase neural regulation?

A

Food in the stomach activates stretch receptors leading to activation of local enteric reflex and activation of the three types of cells

340
Q

Gastric phase vago-vagal reflex?

A

Activated stretch receptord activate the parasympathetic system which sends down efferents for further activation of the ENS and secretory cells

341
Q

Secretagougues?

A

As we start to breakdown food in the stomach we produce secretagogues(amino acids/partially digested proteins) these act on Gastric-Releasing cells which stimulate the parietal cells and release of HCl

342
Q

What is gastrin?

A

A peptide hormone released by endocrine cells in the antrum

343
Q

What activates the G-cells?

A
  1. Secretagogues
  2. Local enteric reflexes(distension in the antrum)
  3. Vagally-mediated reflexes(ago-vagal reflexes)
344
Q

Gastrin released during the cephalic phase ?

A

Vagally mediated release of gastrin occurs during the cephalic phase

345
Q

How does gastrin cause the release of more gastrin?

A
  1. Secretagogues stimulate G-cells releasing gastrin
  2. Gastrin stimulates parietal cells which release HCl
  3. HCl activates pepsinogen and leads to the formation of more secretagogues further activating the G-cells to secrete more gastrin
346
Q

How d G-cells know when to stop releasing gastrin?

A

When the pH falls below 2 G-cells will turn off secretion

347
Q

Role of somatostatin cells?

A

Somatostatin cells are stimulated by low pH and has an inhibitory effect on the G-cells and parietal cells (stops release of both gastrin and HCl)

348
Q

Two functions of Gastrin?

A

-Stimulates HCl secretion by parietal cells
-Stimultate the production of more parietal cells

349
Q

Where is Gastrin released?

A

Stomach + duodenum

350
Q

T/F: There is always a lot of histamine present in the gastric mucosa?

351
Q

What does histamine do to gastric juice?

A

Expels large volumes of gastric juice with lots of HCl

352
Q

What is the common mediator hypothesis?

A

The idea that gastrin and ACh cause the release of histamine which is the final chemostimulator of the parietal cell

353
Q

Why is the common mediator hypothesis wrong?

A

Parietal cells have receptors for ACh, histamine and gastrin which means they all stimulate the parietal cell and not just histamine

354
Q

How does the blockage of one of the receptors(ex. histamine) affect Ach and gastrin?

A

Blockage or stimultation of one of the receptors changes the properties of one or both of the other 2 receptors

355
Q

T/F: ACh, Gastrin and Histamine have cooperative effects?

356
Q

What happens if you block the H2 receptor?

A

Blockage of the H2 receptor prevents histamine from binding to the parietal cell which will decrease the sensitivity of the parietal cell to ACh and gastrin (making it harder to activate)
-Could be used to treat ulcers

357
Q

Initial intesitinal phase of secretion?

A

Initially when secretagogues reach the duodenum they have an excitatory effect and lead to a brief increase in acid production by something similar to gastrin

358
Q

Intestinal phase inhibitory component?

A

Triggers that inhibites peristalsis also inhibit gastric secretion
-Hormones such as secretin and CCK also inhibit gastric secretion

359
Q

Four functions of the upper intestine?

A
  1. Chyme neutralization
  2. Osmotic equilibrium(will be isotonic once it reaches the colon)
  3. Digestion continues
  4. Absorption begins
360
Q

Where do secretions into the small intestine come from?

A
  1. Liver
  2. Gall bladder
  3. Pancreas
361
Q

How do the three secrete into the duodenum?

A

Liver releases enzymes via common bile duct this converges wit hte cystic duct of the gall bladder and then they converg with the pancreatic duct

362
Q

What is the Ampulla of Vater?

A

It is a sweilling where the common bile duct and pancreatic duct converge

363
Q

Role of the sphincter of Oddi?

A

When open we can have secretions from the pancreas, liver and gall bladder at the level of the SI

364
Q

Where are the enzymes of the pancreas made?

A

Mainly come from the head of the pancrease via ducts in the head

365
Q

How much pancreatic juice do we secrete per day?

A

0.5 to 1.5 litres per day

366
Q

Tonicity of the pancreatic juice?

A

Isotonic (trying to neutralize the chyme)

367
Q

Electrolytes in the pancreatic juice?

A

Na+, K+, Cl-, HCO3-(keeps it neutral)

368
Q

pH of the pancreatic juice?

369
Q

T/F: The pancreas produces the largest quantities & the most powerful digestive enzymes?

370
Q

What enzymes does the pancreas produce and how much protein is in them?

A

-3g % protein
-Amylase, Proteases, Lipases

371
Q

T/F: All pancreatic enzymes are released as zynmogen granules?

A

True, they are so powerful that thy would destroy the pancres they are not activated till they reach the duodenum

372
Q

What activates the pancreatic enzyme trypsinogen to trypsin?

A

Enteropeptidase/enterokinase which is only released in the small intestine

373
Q

What happens one trypsin is activated?

A

Trypsin can activate more trypsinogen and trypsin can activate other pancreatic enzymes

374
Q

Trypsin inhibitor?

A

Released by the pancreas(protects the pancreas) and inactivates trypsin

375
Q

Meal prior to the intestines?

A

-meal recued to semi-liquid consistency
-Acidified, osmotic pressure is unchanged limited digestions

376
Q

How much are polysaccharides digested once they reach the intestine?

A

They have only been digested by the salivary amylase, ptyalin, and are disaccharides when entering the intestines

377
Q

How much are proteins digested once they reach the intestines?

A

They have only been digested by gastric pepsin and are still polypeptides when entering the intestines

378
Q

How much are lipids digested once they reach the intestines?

A

They have only been digested by lingual lipase and are Di-, monoglycerides and fatty acids

379
Q

Are any of the macromolecules absrobable once they reach the intestines?

A

No not yet

380
Q

Pro-colipase activation?

A

Pro-colipase is released from the pancreas and is activated by trypsin which converts it to colipase

381
Q

Does the pancreas produce lipases?

382
Q

Role of colipase and pH?

A

Colipase helps to convert triglycerides into fatty acids, Di- & Mono-glycerides
Works at pH 8 (alkaline)

383
Q

Largest gland of the body?

384
Q

Functions of the liver?

A

-Storage
-Synthesis
-Detoxification
-Metabolism

385
Q

How is bile secreted from the liver?

A

Bile is secreted from the hepatic ducts and travels through the common bile duct and is then released into the SI at the sphincter of Oddi

386
Q

How much bile do we secrete per day?

A

0.5 to 1.0 litres per day

387
Q

What is the tonicity of bile and the main ions it is composed of?

A

Bile is isotonic and made up of Na+, K+, Cl- and mostly HCO3- (which neutralizes the chyme)

388
Q

What is the pH of bile?

A

Between 7.8 and 8.2 which helps to neutralize the acidic chyme

389
Q

Do liver secretions contain digestive enzymes?

390
Q

How much of the liver secretions are solid?

391
Q

What are the solids found in liver secretions?

A

-Bile Acids(Bile salts)
-Bile Pigments
-Cholesterol
-Phospholipids

392
Q

What are Bile Pigments?

A

-The hemoglobin breakdown products that give urine and feces their colour

393
Q

T/F: Bile secretion by the liver is continuous?

A

True, the liver is constantly releasing bile

394
Q

When does the bile enter into the small intestine?

A

Intermittently only when the Sphincter of Oddi is open, so after we have a meal

395
Q

How much bile enters the SI per day?

A

About 500 to 700 ml/day

396
Q

Where is the bile stored when the sphincter of Oddi is closed?

A

The bile is stored in the Gall bladder

397
Q

How are bile salts synthesized?

A

In the liver from cholesterol

398
Q

Function of bile salts?

A

-Facilitate digestion, transport, and absorption of FAT(including cholesterol) by forming water-soluble complexes with the fats
-Facilitate transport and absorption of fat-soluble vitamins
-Reduce surface tension and stabalize emulsions that can be acted upon by lipases

399
Q

What vitamins are fat-soluble?

A

Vitamins A, D, E and K

400
Q

Capacity of the gall bladder?

A

50 to 100 ml

401
Q

How does the gall bladder hold so much bile?

A

The gall bladder concentrates bile solids as they come into the gall bladder by removing water from the bile

402
Q

Concentration of solids in the liver bile vs the gall bladder bile?

A

Hepatic bile: 3% solids
Gall bladder bile: 10-20% solids

403
Q

T/F: Bile in the gall bladder has an increased viscosity ?

A

true, because it has a higher concentration of solids

404
Q

How does the gall bladder affect the pH of bile?

A

Hepatic bile: 7.8 - 8.2
Gall bladder bile: 7.0-7.5 (more neutral)

405
Q

Does the gall bladder synthesize bile salts?

A

NO, it just stores and concentrates them

406
Q

What is a Cholecystectomy?

A

Removal of the gallbladder

407
Q

What are gall stones?

A

When cholesterol or pigments precipitate

408
Q

Why do gall stones cause pain?

A

When you have a meal you will have contraction of the gallbladder to release bile, this contraction will be painful due to the precipitates

409
Q

What does it mean when we say Bile salts are amphipaths?

A

They have a hydrophobic and hydrophilic region

410
Q

How do bile salts help fats move through the SI?

A

Since bile salts are amphipaths and fats are insoluble in water/ The bile salts will bind with their hydrophobic sides to the fats and their hydrophilic sides will be incontact with the aqueous environments of the SI this helps the fats move through the small intestine

411
Q

What is a bile salt with a lipid droplet called?

412
Q

What do bile salts help transport through the SI?

A

Fats
-Cholesterol
-Fat-soluble vitamins

413
Q

T/F: bile salts help form stable emulsions?

A

True, they allow the lipid droplet to remain mixed longer with the SI fluids which allows for easier transport

414
Q

Why is it helpful when micelles become smaller and smaller?

A

This makes the fats more easily accesible to lipases which break them down because now there is less surface to volume ratio

415
Q

How much bile salt do we have in our body at a time?

416
Q

How much bile salts do we synthesize per day?

417
Q

How much bile salts are released into the intestines per day?

418
Q

How do we release so much bile per day but only make 0.5 g?

A

We are constantly recycling the bile salts that we have

419
Q

What is Enterohepatic Circulation(EHC)?

A

The idea that most bile salt is reabsorbed into the portal blood and returned to the liver via the EHC

420
Q

Path of bile salts?

A

Liver to GIT then back to LIver

421
Q

How does bile return to the liver from the small intestine?

A

via the hepatic portal vein

422
Q

Intraportal functions of Bile Salts?

A

-Regulate hepatic bile flow from the liver
-Regulate the synthesis of NEW Bile Salts
-Keep cholesterol in solution

423
Q

How do bile salts regulate hepatic bile flow?

A

Through a positive feedback loop
More bile salt returned to the liver(portal blood), the larger the amount of bile that will be secreted by the liver

424
Q

What happens to bile secretion if we remove the ileum?

A

Lose the ability to recycle bile salts and therefore less bile will be secreted

425
Q

How do bile salts regulate the synthesis of new bile salts?

A

Through a negative feedback loop
More Bile Salt returned to the liver(portal blood), the smaller the amount of NEW bile salt that will be synthesized

426
Q

What happens to bile salt synthesis if we remove the ileum?

A

Less bile salts would be returned to the liver which means there would be an increase in bile salt synthesis

427
Q

How do bile salts keep cholesterol from precipitating?

A

Bile salts form micelles with cholesterol to prevent them from aggregating together in the SI

428
Q

How much does the solubility of cholesterol increase in bile?

A

By 2 x 10^6

429
Q

What is the intestinal lumen medium?

A

-The intestinal lumen contains a watery medium which is what makes fats insoluble in it and unable to be targeted by lipases unless with bile salts

430
Q

Bile salts act as detergents?

A

Yes, they help form stable emulsions and assist in the transport of fat and fat-soluble vitamins and allows lipases to act on them

431
Q

Function of bile salts in the colon?

A
  • Inhibits Na+ transport and H2O absorption
432
Q

What happens if the colon absorbs too much H2O?

A

Constipation

433
Q

What happens if we have excess bile salt in the colon?

A

Diarrhea, limits Na+ and H2O absorption

434
Q

Intraportal functions of bile salts?

A

-regulate volume of bile secreted by the liver
-Regulate synthesis of new bile salts

435
Q

Intrahepatic functions of bile salts?

A

-Keep cholesterol in solution

436
Q

Intraintestinal functions of bile salts?

A

-Emulsify & transport fats

437
Q

Intracolonic functions of bile salts?

A

-inhibit too much water absorption

438
Q

How are secretions at the level of the SI, liver and pancrease regulated?

A

Both neurally and hormonally

439
Q

Where are the cells that secrete in the pancreas?

A

They are in the head of the pancreas

440
Q

Two types of cells in the pancreas?

A
  1. Cells that secrete large volume of juice rich in HCO3-
  2. Cells that secrete a small volume of juice rich in enzymes
441
Q

When are the two cells secreted(give example)?

A

Depending on the meal you had the pancreatic secretions differ.
ex. If you have a very acidic chyme you may need more HCO3- cells to secrete. If you have a fatty meal you may need more juice rich in enzymes

442
Q

Cholerestics + example?

A

Agents that cause the liver to secrete a larger volume of bile
ex. Secretin

443
Q

Cholagogues + example?

A

Agents which cause an increase in gall bladder emptying (cause contraction + opeining of sphincter of Oddi)
ex. CCk

444
Q

When the gall bladder is contracted the sphincter of Oddi is…?

445
Q

How digested are polysaccharides after gastric, pancreatic and hepatic secretions?

A

They are now monosaccharides but still not ready to be absorbed

446
Q

How digested are proteins after gastric, pancreatic and hepatic secretions?

A

They are now amino acids, Di and tripeptides but still not ready to be absorbed

447
Q

How digested are fats after gastric, pancreatic and hepatic secretions?

A

They are now mono, diglycerides and FAs and are ready to be absorbed

448
Q

Where is the final step in digestion?

A

It is mediated by intestinal enzymes produced by mucosa at the site where absorption will take place

449
Q

What is in the intestinal juice secreted by the small intestine?

A

-Water
-Mucous
-Ions

450
Q

Brush border enzymes of the small intestine?

A

epithelial cells in the brush border of the small intestine are attached to microvilli and secrete enzymes

451
Q

Mechanical and Chemical digestion of the SI?

A

Mechanical - contraction of muscle (segmentation)
Chemical - Chyme mixes with pancreatic juice, intestinal juice and bile

452
Q

T/F: SI recieves pancreatic juice enzymes to aid digestion?

453
Q

How does the SI have increased SA?

A

Through crypts and villi

454
Q

What does increased SA aid with in the SI?

A

Secretion, Digestion and Absorption

455
Q

What occurs in the crypt region of the SI?

A

Fluid secretion

456
Q

What are enterocytes?

A

The epithelial cells that cover the microvilli where absorption and secretion are completed

457
Q

Crypt Cells?

A

-Lack digestive enzymes but secrete a large volume of alkaline fluid known as Succus Entericus

458
Q

How much succus entericus do crypt cells secrete?

A

-3 litres per day

459
Q

What does the Succus Entericus do?

A

Neutralizes tonicity and pH of the contents of the lumen

460
Q

Tonicity of Succus Entericus and components?

A

Isotonic and made up of Na+, K+, Cl- and HCO3- (rich in bicarbonate)

461
Q

pH of Succus Entericus?

462
Q

Do villi secrete fluid?

463
Q

Role of villi cells in the SI?

A

Complete digestion and absorb nutrients/fluid

464
Q

Small intestine enzymes that remain in the brush border?

A

-Enterokinase
(activates tyrpsinogen to trypsin)

465
Q

Do enterocytes synthesize digestive enzymes?

A

Yes, but they remain in the brush border

466
Q

What does enterokinase in the SI do?

A

Activates trypsinogen

467
Q

Describe villi cell turnover?

A

Cells in the villi region of the SI apoptose and slough off into the lumen of the SI as cells in the crypt region migrate up to the villus region

468
Q

Cell turnover rate in the villi?

469
Q

Why is cell turnover important in the small intestine?

A

Helps the GIT maintain its function at a high rate removes any cells that have been damaged by movement or acid

470
Q

How are carbohydrates and sugars absorbed into the small intestine?

A

The villi have capillary loops in them, oxygenated blood flows through them and carbohydrates and sugars are absorbed into the loop and sent to the liver via the hepatic portal vein

471
Q

How are fats absorbed into the small intestine?

A

Under the capillary loop there is a lacteal which contains lymph fats are absorbed into the lacteal and are sent to the lymphatic system

472
Q

Digestion and absorption are completed in…

A

The small intestine

473
Q

Does the colon secrete a lot of fluid?

A

NO, only a small volume

474
Q

What type of secretion does the colon secrete?

A

Alkaline and filled with lots of mucin (for feces formation and movement)

475
Q

Does the colon secrete digestive enzymes or absorb nutrients?

476
Q

Bacteria in the colon?

A

The colon is filled with bacteria and their activity must be contained in the colon

477
Q

Regulation of intestinal secretions?

A

-Local enteric reflexes
-Vago-vagal reflexes
-Hormonal factors

478
Q

On average how much water and solids do we consume per day?

A

2000 mL of H2O
500 g of solids

479
Q

On average how much water and solids do we excrete per day and what composition are the solids?

A

50 g of solids
(30% bacteria, 30% undigested fiber, 10-20% lipids, 10-20% inorganic matter)
100 mL of H20

480
Q

Daily secretions into the GIT?

A

Salivary glands: 1500ml
Stomach: 2500 ml
Bile: 500 ml
Pancreas: 1500 ml
Intestine: 1000 ml

481
Q

Total scecretions into the GIT on the daily?

482
Q

How much fluid must be absorbed by the GIT per day to maintain homeostasis?

A

9 litres
(7 from secretions and 2 from ingestion)

483
Q

How much protein is released into the GIT via secretions and must be absorbed?

A

50g as enzymes and 30g as cells
A total of 80g of protein is secreted into the GIT these 80g must all be absorbed and recycled into amino acids

484
Q

T/F: The majority of absorption in the GIT is reabsorption?

485
Q

Sites of exchange in the small intestine are characterized by..?

A
  1. Very large surface area of small intestine
  2. Intimate contact with blood vessels(capillary loops)
486
Q

Only GI organ essential to life?

A

The small intestine

487
Q

What aspects of the SI greatly increase its surface area?

A

Circular folds, villi and microvilli all contribute to a greater surface area

488
Q

Postprandial blood flow to the intestine?

A

1-2 liters per minute, large flow of blood is critical for absorption of nutrients

489
Q

Lymph flow in the small intestine?

A

1-2 ml/minute, lipids flow slower than sugars and carbohydrates

490
Q

Where in the SI is iron and Ca++ absorbed?

A

The duodenum

491
Q

Where in the SI are carbohydrates absorbed?

A

Throughout the entire small intestine

492
Q

Where in the SI are proteins, lipids, Na+ and H2O absorbed?

A

Throughout

493
Q

Where in the SI is vitamin B12 absorbed?

A

The distal illeum

494
Q

Where in the SI are bile salts absorbed?

A

They can be absorbed throughout the entire SI but are mainly abosrbed at the illeum since they are still in use till then

495
Q

How does absorption take place in the small intestine?

A

-Simple diffusion
-Facilitated diffusion
-Active transport
-Pinocytosis

496
Q

Most important method of absorption in the small intestine?

A

-Osmosis, for everything that comes in water has to come in as well this is how we are able to absorb all 9 litres of fluid

497
Q

What limits absorption in the SI?

A

-Adequate digestion(enzymes, pH)
-Adequate sites for absorption
-Adequate transit time for absorption
-Adequate Co-factors, transporters

498
Q

How much fluid is absorbed at the SI vs the colon?

A

The SI absorbs 7 litres of fluid
The colon absorbs 2 litres of fluid (only bring in ions)

499
Q

Maximum absorption capacity of the SI and colon?

A

Small intestine: 15 litres/day
Colon: 4-5 litres/day

500
Q

Lactose intolerance?

A

When you are missing the lactase enzyme and cannot breakdown lactose.
Lactose stays in the SI and is acted on by bacteria in the colon causing bloating/pain

501
Q

Chylomicrons?

A

Fats are absorbed through the lipid membrane and then they complex with proteins to form chylomicrons and then they move into the lacteal

502
Q

How is the GIT transit time determined?

A

The GIT transit time is related to the functional activities of each organ (the more activity the organ does the longer the transit time)

503
Q

Transit time in the mouth, esophagus and stomach?

A

Mouth: 1 second
Esophagus: Seconds
Stomach: Minutes - Hours

504
Q

Transit time in the small intestine and colon?

A

SI: Several hours
Colon: Hours - Days

505
Q

List all of the protective mechanisms of the GIT?

A
  1. Mucin
  2. Inactive Proteases, Trypsin Inhibitor
  3. Gastric Mucosal Barrier
  4. Sphincters prevent reflux
  5. Negative feedback inhibition of gastrin
  6. Neutralization of duodenal contents
  7. Myogennic Motor Complex