GI Lecture 1-3 Flashcards

1
Q

What is the GI tract?

A

concentric muscle cylinders lined with an epithelium.

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2
Q

What are the accessory organs?

A

Teeth, tongue, salivary glands, liver, pancreas

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3
Q

What are identifying characteristics for the carnivorous GI tract?

A

A big stomach
and a relatively short
intestinal tract. They must eat a lot before other competitors arrive. Slower absorption.

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4
Q

What are identifying characteristics for the ruminant GI tract?

A

fermentation in
the fore stomach system

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5
Q

What are identifying characteristics for the equine GI tract?

A

fermentation in the
large intestine. (Small stomach, large intestine is fermentive)

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6
Q

What are identifying characteristics for the Bird GI tract?

A

food store (the crop),
a glandular stomach (pro-
ventriculus), and a
muscular stomach (gizzard)

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7
Q

What are the major functions of the GI tract?

A
  • Transportation of food
  • Digestion
  • Absorption
  • Regulation (H2O and electrolyte balance)
  • Immunologic Barrier (GALT)
  • Thermoregulation
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8
Q

What is prehension?

A

How food is grabbed.
Species differ in feeding behavior

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9
Q

How does prehension occur in Horses?

A

lips (when eating from manger) or incisors (when grazing)

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10
Q

How does prehension occur in Cattle?

A

tongue (wrap the tongue around forage) and incisors

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11
Q

How does prehension occur in goat and sheep?

A

tongue and lips

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12
Q

How does prehension occur in pigs?

A

snout and mandible

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13
Q

How does prehension occur in carnivorous animals?

A

canines, incisors, and forelimbs

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14
Q

What is mastication?

A

The first act of digestion, involves the actions of the teeth, jaws, tongue, and cheeks

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15
Q

What are the key features of mastication in carnivorous animals?

A

very sparsely, movement of the mandible are vertical. Molars and
premolars in the upper and lower jaws move against each other like scissor blades

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16
Q

What are the key features of mastication in herbivorous animals?

A

spend long time masticating, upper and lower jaws are large providing
room for teeth with large chewing surfaces. Mastication movements are horizontal
Ruminants —-> Regurgitation, Remastication

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17
Q

What are the functions of movements of the GI tract?

A

 To propel ingesta from one location to the next
 To retain ingesta at a given site for digestion, absorption, or storage
 To break up food material physically and mix it with digestive
secretions
 To circulate ingesta so that all portions come in contact with
absorptive surfaces
-

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18
Q

What kind of meal moves through the GI tract quicker, a hypocaloric meal or a hypercaloric one?

A

Hypocaloric- less to digest

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19
Q

What is Deglutition?

A

The first motility pattern in the GI tract is the deglutition Deglutition involves voluntary and involuntary stages and occurs after food has been masticated

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20
Q

What occurs in the voluntary phase (oral phase) of deglutitation?

A

Food is in the oral cavity and is molded into a bolus Using the tongue it will be pushed back into the pharynx
When food enters the pharynx
-> activation of sensory nerve endings ->initiation of the involuntary part of deglutition

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21
Q

What occurs in the involuntary phase (swallow reflex) of deglutitation?

A

Involuntary phase (swallow reflex): It occurs within the pharynx and esophagus -> it directs food into the digestive system (away from the upper airways)

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22
Q

What occurs step by step during deglutition?

A
  • soft palate closes pharyngeal opening of nasopharynx
  • tongue is pressed against hard palate to close oral opening.
  • epiglottis is moved backwards, covering the entrance of trachea.
  • upper esophageal sphincter opens and peristaltic contractions allows food to move through esophagus and trachea reopens and respiration continues
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23
Q

What are some disorders of deglutition?

A

Dysphagia which can result from neuromuscular disorder or mechanical obstruction.

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24
Q

What are the classification of Dysphagia?

A
  • oropharyngeal dysphagia: due to malfunction of the pharynx and upper esophageal
    sphincter (Parkinsons)
  • esophageal dysphagia: due to malfunction of the esophagus (ex: megaesophagus)
  • Aspiration: a dysphagia in which food particles /fluids or stomach contents (acid reflux)
    reach the upper airways
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25
Q

What is the regulatory center for energy homeostasis?

A

Hypothalamus

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26
Q

What is within the hunger center?

A

Nucl. Paraventricularis, lateral hypothalamus fields, perifornical region

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27
Q

What is within the satiety center?

A

Nucl. ventromedialis

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28
Q

What are stimulatory neuropeptides (Hunger) from the hypothalamus?

A

Neuropeptide Y (NPY) and Orexin

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29
Q

What are inhibitory (Satiety) neuropeptides from the hypothalamus?

A

Melanocyte-stimulating hormone (MSH)
Think of the labradors!

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30
Q

What are stimulatory (Hunger) non-hypothalamic hormones?

A

Ghrelin

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31
Q

What are inhibitory (Satiety) non-hypothalamic hormones?

A

Cholecystokinin (CCK), Peptide YY (PYY), Leptin (fat cells -> inhibits NPY release and activates MSH release and activity), Insulin (pancreas -> glucose availability)

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32
Q

What are the major salivary glands?

A
  • Parotis (parotid gland)
  • Mandibularis (mandibular gland)
  • Sublingualis (sublingual gland
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33
Q

What are the small salivary glands?

A
  • Ventral jaw glands
  • Palate, pharyngeal glands
  • Lips glands (labiales)
  • Zygomatic glands
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34
Q

Which salivary glands provide the largest amount of secretion?

A

Parotis and Mandibularis account for 90% of salivary secretion

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35
Q

What is the primary function of saliva (digestive)?

A

 Protection of the buccal mucosa and teeth
 Facilitation of deglutition
 Initiation of enzymatic carbohydrate
digestion (human and pigs -> amylase) -> pH regulation (HCO -)

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36
Q

What are the secondary functions of saliva?

A

• Immunologic function (Lysozyme, Ig‘s)
• Thermoregulation (panting in dogs)
• Defense mechanism in some species (llamas,
alpacas)

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37
Q

What makes up saliva?

A

99% Water and 1% electrolytes (Na+, K+, Cl-, HCO3-)

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38
Q

In the salivary gland, what is produced in the ducts?

A

Secondary Saliva (K+, and HCO-)

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39
Q

In the salivary gland, what is produced in the acinus?

A

Primary Saliva (Cl-, Na+. H2O)

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40
Q

What can be caused by disturbances in saliva production?

A
  • Xerostomia (dry mouth)
  • buccal ulcers
  • dysphagia
  • proliferation of bacterial population
  • Cavities
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41
Q

What are the four routes secretions of the Gi tract reach their target tissue?

A
  • Endocrine
  • Paracrine
  • Autocrine (not hormones, does not enter blood)
  • Neurocrine
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42
Q

What is Neurocrine secretion?

A

secretions by enteric neurons that affect muscle cells, glands, and blood cells.

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43
Q

What is Autocrine secretion?

A

Secretions of a given cell regulate functions of the same cell.

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44
Q

What is paracrine secretion?

A

Secretions that diffuse through the interstitial space to affect other cells.

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45
Q

Where is secretin synthesized?

A

Duodenum, Jejunum

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46
Q

Where is Gastrin Synthesized?

A

Antrum, Duodenum

47
Q

Where is CCK synthesized?

A

Duodenum, Jejunum, Ileum

48
Q

Where is GIP synthesized?

A

Duodenum and Jejunum

49
Q

Where is Motilin synthesized?

A

Duodenum and Jejunum

50
Q

What is the action of secretin? What is its stimulants?

A

Stimulates bicarbonate secretion Acid, fat, and protein
and inhibits acid secretion
Stimulants: Acid, fat, and protein

51
Q

What is the action of Gastrin? What is its stimulants?

A

Stimulates acid secretion.
Stimulants: Protein, high pH

52
Q

What is the action of CCK? What is its stimulants?

A

Stimulates pancreatic enzyme secretion and gallbladder contraction.
Stimulants: Fats and proteins

53
Q

What is the action of GIP? What is its stimulants?

A

Inhibits gastric secretion and stimulates insulin secretion
Stimulants: Fats and glucose

54
Q

What is the action of motilin? What is its stimulants?

A

Induction of intestinal motility during fasting (MMC)
Stimulants: Acetylcholine
Rest and digest

55
Q

What are the 4 sections of the monogastric stomach?

A

Cardias, Esophogeal, Fundus and Corpus, Pylorus

56
Q

Which section of the monogastric stomach is larger in horses?

A

Esophageal

57
Q

Which section of the monogastric stomach is larger in pigs?

A

Cardia

58
Q

What are the three glandular zones of the stomach? What are their secretions?

A

Cardias - Mucus
Fundus- HCl, Enzymes
Pylorus- Mucus

59
Q

What are gastric pits?

A

Gastric folds

60
Q

What do parietal cells secrete and what is their location?

A

located in the neck of the gastric gland, and secrete HCl and Parietal cells secrete Instrinsic Factor

61
Q

What do chief cells secrete?

A

secrete proteolytic enzyme precursors such as pepsinogen

62
Q

What are mucus neck cells? What do they secrete?

A

They are progenitor cells for gastric mucosa. They secrete thin mucus unless they differentiate into one of the other cells. STEM CELLS

63
Q

What is the importance of intrinsic factor secreted by Parietal cells?

A

Essential for vit. B12 Mucus
Gastric gland
mucous cells
absorption in the ileum

64
Q

What does enteroendocrine cells secrete?

A

They secrete hormones like Gastrin, GIP, ect

65
Q

Why is HCl important in nature?

A

Acid is important to start digestion. Animals that eat bone also need HCl to break down the bone and demineralize it so it will not cause any issues and can be digested.

66
Q

What are proenzymes?

A

Proenzymes are are forms enzymes that dont destroy the cells.

67
Q

What does enteroendocrine cells secrete?

A

G cells - Gastrin
D cells- Somatostatin
I cells- CCK

68
Q

Where do entoendocrine secrete their granule content, and where do they go from there?

A

They secrete their granule contents into the lamina propria. Some will reach blood capillaries after that.

69
Q

What are mucins?

A

glycoproteins) are secreted by exocytosis

70
Q

How long do surface mucus cells live?

A

Surface mucous cells do not live long (regeneration every 3-5 days (↑ mitotic activity in the isthmus of the gastric pit)

71
Q

What are the purpose of mucus cells?

A

Protection and lubrication of the mucosa.

72
Q

What are the three levels that regulate HCL secretion?

A

Neural (acetylcholine)
Hormonal (Gastrin)
Paracrine (Histamine

73
Q

What secretes the each of the mediators for HCl secretion regulation?

A

acetylcholine- vagus nerve
histamine - enterochromatin like cells.
gastrin- vagus nerve

74
Q

At what pH is HCl production inhibited?

A

< 3

75
Q

What kind of feedback mechanism is the HCl secretion of parietal cells?

A

Negative feedback mechanism

76
Q

What is released from D cells that inhibits Gastrin production?

A

Somatastatin

77
Q

What occurs in the apical membrane after acid secretion?

A

Canaliculi fuse with the apical (luminal) membrane and vesicles containing H+/K+ ATPase are targeted to the apical membrane increasing HCl secretion

78
Q

What is released from the small intestine when food particles are present?

A

CCK and Secretin

79
Q

What is the reason that NSAIDS would cause gastric ulcers?

A

NSAIDs block COX 1 and COX 2, which normally leads to the formation of prostaglandins and leukotrines. Without these mucus production decreases and a gastric ulcer can form.

80
Q

TRUE or FALSE: After 3 days on NSAIDS a generally healthy patient is at high risk for a gastric ulcer

A

FALSE
It would be with long term use of NSAIDs

81
Q

What else does removing COX 1 cause and how can it further worsen gastric ulcers?

A

Impairs healing via reduced mucosal blood-flow, impaired platelet aggregation and increased bleeding/ injury

82
Q

What else does removing COX 2 cause and how can it further worsen gastric ulcers?

A

Reduces angiogenesis and reduces leukocyte adherence and increases leukocyte activation which could cause further damage and decrease healing.

83
Q

What is the pH of gastric acid?

A

(1-4)

84
Q

How does H. Pylori evade being destroyed by the Gastric acid?

A

H. Pylori burrows under the mucosal layer and produces urease which neutralizes acid pH, thus making the environment more bacteria friendly. This also will destroy mucus production and the stomach acid will destroy the gi cells.

85
Q

What is the pH in the proximal part of the stomach in horses and pigs?

A

4-6

86
Q

Prochymosine is broken down to what? Where? And by who?

A

In calves and lambs Prochymosine is broken down to chymosine in the abomasum, where hydrolysis of milk protein occurs.

87
Q

Pepsinogen is broken down to what?

A

Pepsin

88
Q

What can cause gastric ulcers in horses? Why?

A

*Bacteria can colonize the proximal part of the stomach, and cause hydrolysis of carbohydrates in short chain fatty acids and lactate. This will create a more acidic pH and will cause damage to the mucosa, hence gastric ulcer.
- Stress can be a reason horses are more susceptible to gastric ulcers, not eating

89
Q

What are the three phases to gastric secretions?

A

Cephalic
Gastric
Intestinal

90
Q

What occurs during the cephalic phase of digestion?

A

Sight, smell, thought, or taste, the greater the appetite the stronger the stimulation.
- Stomach acid is increased due to chief cells releasing pepsinogen and parietal cells secreting HCl because of nerve impulses from vagal nerve. Gastrin is in blood and indicates the need for more HCl release from parietal cells to prepare for digestion.

91
Q

What occurs during the Gastric phase of digestion?

A

Induced by vasovagal reflexes from stomach to the brain ( via stomach dialation/ presence of amino acids and peptides in gi lumen)

Presence of peptides inn stomach —> cause gastrin producing cells to generate gastrin in the blood which increases the secretion of parietal cells and chief cells to make hcl and pepsinogen respectively.

92
Q

What occurs during the Intestinal phase of digestion?

A

Induced by the presence of food in the duodenum (it works as a feedback).

Food makes it to the duodenum and this causes the cycle to repeat due to the presumption more food is going to be coming through the stomach.

93
Q

What are the three levels of surface convolutions of the small intestine to expand surface area?

A

Plicae circulares (in some species), Villi, and microvilli.

94
Q

What are the names of the gland like structure at the base of the villi of the small intestine?

A

crypts of Lieberkühn

95
Q

What is the secretions of paneth cells?

A

antimicrobial enzymes and peptides

96
Q

What is the function and secretion of mature enterocytes/ absorptive cells?

A

Function: absorption of nutrients
Secretion: digestive enzymes as well as water, Cl-, and HCO3

97
Q

What are the secretions of Goblet cells?

A

secretion of mucus

98
Q

What are the secretion of enteroendocrine cells?

A

hormones such as CCK, secretin, and GIP

99
Q

What are brunners glands? What is their function? What do they Secrete?

A

Tubulo alveolar glands (submucosa)

Secretion of mucus through exocytosis

Brunner glands also secrete glycoproteins and bicarbonate ions (pH of Brunner glands‘ secretion is 8.1 – 9.3)

Function: protection of small intestine mucosa by neutralizing the acid- containing chyme delivered to it from the stomach

100
Q

Where do division and replication of enterocytes occur?

A
  • occurs in the crypts only
    Intestinal crypt cells are among the most rapidly regenerating cells of the body
101
Q

What is the turnover time of enterocyte regeneration?

A

4-7 days

102
Q

What determines the length of the villi in the small intestine?

A

The length of villi is determined by the rate at which cells are lost at the tips and at the rate at which they are replaced. An increase in cell loss at the villi tips, relative to the crypt cell replication, results in shortening of the villi

103
Q

When the proginator cells are differentiated into the needed cell, what occurs? What is the exception?

A

The cell will migrate up the villi. Paneth cells will migrate down into the crypt and reside between crypt base columnar cells.

104
Q

What is the mediator of water secretion in the small intestine?

A

All water secretion in the intestine is mediated by osmosis

105
Q

What can cause food to be hyperosmotic and how does the small intestine accomodate for that?

A

Food entering the intestine may be hyperosmotic (salty foods and foods with high sugar contents) or become hyperosmotic after digestion (starchy meal); osmotically active substances draw water from the lateral spaces into the intestinal lumen

106
Q

As solutes are absorbed in the small intestine, how does water move?

A

water follows them osmotically back through the epithelium and into the vascular system reaching the blood stream

107
Q

In general what direction does water move in the small intestine?

A

Water will move in whatever direction to keep the ingesta isoosmotic.

108
Q

What are components/ important information about the large intestine?

A
  • Microbial metabolism (significant in horses and rabbits)
  • One layer cylindric epithel (crypts are also present)
  • Water absorption, vitamins
  • Goblet cells -> mucus

Secretion: small volumen, isoton to
plasma, mucin, bicarbonate and potassium rich (alkaline)

109
Q

What is a large difference between mucosa within the small intestine and the mucosa of the large intestine?

A

The mucosa is composed of crypts but not villi lined by goblet cells (mucus) and some absorptive epithelial cells (absorption of some electrolytes and water)

110
Q

Where do water and nutrients go before entering the vascular system?

A

Water and nutrients enter first the extracellular fluid
before entering the vascular system

111
Q

What forces are responsible for driving the movement of solutes and water between intravascular and extravascular fluids?

A

oncotic and hydrostatic forces.

112
Q

How do absorbed nutrients enter the capillaries?

A

Absorbed nutrients enter then the capillaries by
diffusion from the interstitium (this drives water to the
capillaries too)

113
Q

Where does venous blood from the GI tract collect?

A

The hepatic portal vein and passes through the liver before entering the vena cava and returning to the heart.

Not including the terminal colon and rectum

114
Q

TRUE OR FALSE: Lymphatic drainage from the gut passes through the liver and then is reentered into circulation.

A

FALSE- Lymphatic drainage from the gut bypasses the liver entering the bloodstream through the thoracic duct