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Physiology II > Exam # 1 ( GI 1-5) > Flashcards

Exam # 1 ( GI 1-5) 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

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47
Q

Where is CCK synthesized?

A

Duodenum, Jejunum, Ileum

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48
Q

Where is GIP synthesized?

A

Duodenum and Jejunum

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49
Q

Where is Motilin synthesized?

A

Duodenum and Jejunum

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50
Q

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

A

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

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51
Q

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

A

Stimulates acid secretion.
Stimulants: Protein, high pH

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52
Q

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

A

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

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53
Q

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

A

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

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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

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55
Q

What are the 4 sections of the monogastric stomach?

A

Cardias, Esophogeal, Fundus and Corpus, Pylorus

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56
Q

Which section of the monogastric stomach is larger in horses?

A

Esophageal

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57
Q

Which section of the monogastric stomach is larger in pigs?

A

Cardia

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58
Q

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

A

Cardias - Mucus
Fundus- HCl, Enzymes
Pylorus- Mucus

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59
Q

What are gastric pits?

A

Gastric folds

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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

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61
Q

What do chief cells secrete?

A

secrete proteolytic enzyme precursors such as pepsinogen

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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

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63
Q

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

A

Essential for vit. B12 absorption in the ileum

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64
Q

What does enteroendocrine cells secrete?

A

They secrete hormones like Gastrin, GIP, ect

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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.

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66
Q

What are proenzymes?

A

Proenzymes are are forms enzymes that dont destroy the cells.

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67
Q

What does enteroendocrine cells secrete?

A

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

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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.

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69
Q

What are mucins?

A

glycoproteins) are secreted by exocytosis

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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)

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71
Q

What are the purpose of mucus cells?

A

Protection and lubrication of the mucosa.

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72
Q

What are the three levels that regulate HCL secretion?

A

Neural (acetylcholine)
Hormonal (Gastrin)
Paracrine (Histamine

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73
Q

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

A

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

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74
Q

At what pH is HCl production inhibited?

A

< 3

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75
Q

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

A

Negative feedback mechanism

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76
Q

What is released from D cells that inhibits Gastrin production?

A

Somatastatin

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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

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78
Q

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

A

CCK and Secretin

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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.

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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

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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

115
Q

What can you find in the liver lobule?

A

Portal venules, arteriole of hepatic artery, bile duct.

116
Q

What kind of capillaries are found in the liver? Why?

A

Sinusoidal ( this is to allow proteins and large solutes to enter the blood)

117
Q

What are the functions of the liver?

A
  • Carbohydrate metabolism (gluconeogenesis, glycolysis)
  • Amino acid and protein metabolism (synthesis of plasma proteins)
  • Lipid Metabolism ((fatty acids oxidation, ketone bodies synthesis)
  • Storage (glycogen, lipids, vitamins, copper, iron)
  • Synthesis and secretion of bile acids, bile formation
  • Biotransformation (medicaments, xenobiotics, metabolism byproducts)
  • Synthesis of hormones and mediators
  • Synthesis of components of the immune system
118
Q

What are the components the liver produces that is part of the plasma protein?

A

◦ Albumins
◦ Lipoproteins:
‣ VLDLs
‣ LDLs
‣ HDLs
◦ Glycoproteins: haptoglobin, transferrin
◦ Prothrombin and fibrinogen
◦ Non-immune alfa- and beta-globulins

119
Q

What are VLDLs and what do they do?

A

Lipoproteins: They transport triglycerides from liver to the other organs.

120
Q

What are LDLs and what do they do?

A

Lipoproteins: They transport cholesterol esters from liver to the peripheral tissues. (bad cholesterol)

121
Q

What are HDL’s and what do they do?

A

Lipoproteins: They remove cholesterol from the peripheral tissues and transports it to the liver. (good cholesterol)

122
Q

What hormones are synthesized in the liver? What are they?

A
  • Angiotensinogen -> Prohormone
  • Thrombopoetin -> Hormone (Growth factor)
  • IGF (Insulin-like growth factors) -> IGF 1 and 2
  • Hepcidin -> Small peptide hormone (iron homeostasis)
123
Q

What is biotransformation?

A

• Group of reactions involved in the conversion of toxic molecules in non-toxic, water soluble and more excretable substances.

124
Q

What is important about most drugs that we can give to patients?

A

• Most drugs are liposoluble (and would, therefore, stay long in the body). Biotransformation is essential for the termination of their action and their elimination from the body

125
Q

What is the largest site for biotransformation?

A

The liver

126
Q

What are the enzymes involved in biotransformation in the liver?

A

Cytochrome P450 enzymes

127
Q

TRUE or FALSE: Drug Metabolism leads to increased polarity

A

True

128
Q

What does increased polarity mean in terms of drug metabolism?

A

makes drugs and their metabolites more water soluble

129
Q

How many phases are involved in biotransformation?

A

2

130
Q

What occurs in phase one of biotransformation?

A

Phase I - (oxidation+ Hydroxylation (adding -OH group) + Carboxylation (adding -COOH group) to a foreign compound. This is performed in the sER and the mitochondria (reactions with proteins called cytochrome P450)

131
Q

What occurs in phase two of biotransformation?

A

Phase II- called conjugation, addition of glucuronic acid, glycine or taurine to the target substance. Makes the product of phase one more water soluble so it can easily be eliminated.

132
Q

Where is bile produced?

A

The bile is produced in the hepatocytes and is modified in epithelial cells of the gallbladder.

133
Q

What is the role of the Gall bladder?

A

Gallbladder: Storage and concentration through electrolyte and water resorption.

134
Q

What is synthesized to make bile acid?

A

Bile acids are synthesized from cholesterol and conjugated with amino acids ( glycine, taurine)

135
Q

What is bile acids, and where are they secreted?

A

Bile acids are amphipathic molecules and most important component of bile. They are secreted into the duodenum where they emulsify fat droplets in small intestine.

136
Q

When bile acids are secreted into the duodenum and emulsify fat droplets in the small intestine, what is formed?

A

Forming mixed micelles

137
Q

What is the path of bile in the liver?

A

Bile is excreted into bile canaliculi ( small canals between hepatocytes). Bile canaliculi gradually feed into larger canals and then into common bile duct (ductus choledochu)

138
Q

What is the muscle that prevents bile from leaking into the duodenum?

A

• Sphincter of Oddi (smooth muscle)

139
Q

When there is no digestion, where is bile stored?

A

gallbladder.

140
Q

What causes oddi’s sphincter to relax and release bile?

A

• After meal gallbladder is emptied:
◦ increased amino acids and fatty acids in duodenum-> Increased CCK -> contraction of smooth muscle and relaxation of Oddi’s sphincter.

141
Q

What is the refractory mechanism that affects the circulation of bile?

A

Refectory -> increased Ach -> contraction of the smooth muscle.

142
Q

What is the components of bile?

A

Bile acids, Bile pigment, phospholipids, cholesterine, Na+, K+, Ca++, Cl-, HCO3-

143
Q

What is the pH of bile?

A

8.2

144
Q

What is the general steps of synthesis and circulation of bile acids?

A

Cholesterol within hepatocytes interact with bile acids, this then goes through transporters that transport the bile into the bile caniculi, where the bile is then fed into the bile duct and eventually is released into the duodenum. The bile acids are reabsorbed through the intestinal lumen in the ileum through a sodium transporter, and then they go through an additional transporter into the bloodstream. This then transports back through to the liver where the bile is collected for reuse.

145
Q

What percentage of bile is made each time we eat? How much is recirculated?

A

95 % is recirculated, 5% is what is made de novo in the liver.

146
Q

What are the two tissues that compose the pancreas and what do they each secrete?

A

• Pancreas is composed of two functionally separate types of glandular tissues, the endocrine (secretion of hormones) and the exocrine pancreas (secretion of digestive enzymes)

147
Q

What is the exocrine pancreas?

A

The exocrine pancreas is an acinar gland connected by arborizing system of ducts.
◦ Structure of exocrine pancreas resembles the salivary gland

148
Q

What is the secretion in the acinus of the exocrine pancreas made of?

A

• Secretion in acinus resembles the primary saliva (i.e Cl- channel apical; Na+/K+/2Cl- cotransporter basolateral);

149
Q

In the exocrine pancreas, where does the addition of HCO3- occur?

A

In the ducts.

150
Q

What are zygomens?

A

Inactive forms of proteases which are not going to harm the pancreatic cells.

151
Q

What digestive enzymes are produced in the pancreas?

A

‣ Peptidases (produced in inactive form): Trypsinogen, chymotrypsinogen, proelastase, procarboxypeptidase A and B.
‣ Nucleases: Ribonuclease, desoxyribonuclease
‣ Amylases: alpha- amylase
‣ Lipases

152
Q

What receptors do pancreatic cells have?

A

• Pancreatic cells have receptors for acetylcholine, CCK, and secretin

153
Q

How can diet effect the concentration of specific digestive enzymes?

A

◦ increased starch —–> Increased amylase
◦ Increased fat and protein —-> Increased lipases and peptidases.

154
Q

What are the phases of regulation for the exocrine pancreas?

A

Regulation:
◦ Cephalic phase (site, smell, imagination)
◦ Gastric Phase (dilation of the stomach)
◦ Intestinal Phase

155
Q

What occurs in the intestinal phase of regulation of the exocrine pancreas?

A

‣ decrease in pH –> increase secretin) (this is to balance the ph and keep it from becoming too acidic and damage the intestines)
‣ Increase in AA, FF —-> increase in CCK

156
Q

What are two examples of impairment of pancreas secretion?

A
  • Pancreatic insufficiency
  • Pancreatitis
157
Q

What is pancreatic insufficiency? What is the clinical signs?

A

◦ Insufficient production of digestive enzymes by the exocrine pancreas; mal digestion;
◦ Clinical signs: Greasy/oily stools (steatorrhea), polyphagia, rapid weight loss

158
Q

What is pancreatitis? What is the clinical signs?

A

◦ In dogs relatively frequent (middle to old age, obese dogs); acini destroyed and replaced by connective tissues because of auto-digestion Increased risk when eating too much fat, human food or garbage

159
Q

What does secretin stimulate?

A

Production of a bicarbonate rich secretion

160
Q

What does acetylcholine and CCK stimulate?

A

Secretion of an enzyme and chloride rich fluid.

161
Q

What is the active form of trypsinogen?

A

Trypsin

162
Q

What does it mean to be amphipathic?

A

One side of compound hydrophilic, one side hydrophobic.

163
Q

When does the reflectory response within the bile duct occur?

A

can occur just before eating.

164
Q

What is the pathway of bile acids?

A

Bile acids within the bile in the gallbladder is released into the small intestine via the bile duct. The bile acids are absorbed via the intestinal lumen and then will be absorbed into blood stream where it is returned to the liver through the hepatic portal vein.

165
Q

What causes the conversion of trypsinogen to Trypsin? Where is it activated?

A

enteropepsidase. In the duodenum

166
Q

During an episode of pancreatitis what occurs to the zymogens that causes local damage of pancreatic cells?

A

During pancreatitis, the zymogen granules and lysosomes can fuse, and their contents can mix together in intracellular vacuoles, leading to premature, increased, intracellular activation of zygomens. Such abnormal activation leads to local damage of pancreatic cells

167
Q

What can occur in pancreatitis when trypsinogen, trypsin, and zymogens are prematurely activated?

A

Additionally, if there is premature intracellular activation of trypsinogen, trypsin, and zymogens, this causes additional activation of other zymogens, thus leading to additional pancreatic damage.

168
Q

What inflammatory mediators are released during an episode of pancreatitis?

A

Many inflammatory mediators are also released, including TNF-alpha, IL-1, IL-2, IL-6, IL-8, IL- 10, IFN-alpha, IFN-gamma, and platelet activating factor

169
Q

What can the release of inflammatory mediators cause in a patient with pancreatitis?

A

This can lead to shock, disseminated intravascular coagulation (DIC), and death

170
Q

What usually activates zymogens?

A

They are activated by cleavage of the amino-terminal polypeptide chain. Zymogens are normally not activated until they reach the small intestine.

171
Q

What is the treatment of pancreatitis?

A

Stabilization of patients with fluid/electrolyte therapy is recommended. Additionally, analgesics and antibiotics are often recommended. Both parenteral and enteral feeding, after vomiting ceases, have been recommended

172
Q

What is the prognosis of a patient with pancreatitis? What causes it? Who is more susceptible?

A

Overweight dogs are more susceptible. There is no known/ definitive cause. Prognosis varies, depending on cause, severity, and chronicity of disease.

173
Q

What are the functions of carbohydrates in the body?

A

Functions:

  • Energy source
  • Storage form of energy
  • Cell membrane component (communication)
  • Structural component (cell wall of bacteria)
174
Q

What are carbohydrates made from?

A

All carbohydrates are made from monosaccharides

175
Q

Monosacharides are categorized based on what?

A

Monosaccharides (simple sugars) are categorized according to the number of carbons

177
Q

TRUE OR FALSE: Carbohydrates are the most abundant organic molecules in nature.

A

TRUE

178
Q

What are disaccharides?

A

Monosaccharides linked by glycosidic bonds

179
Q

What are oligosaccharides?

A

3-10 Monosaccharides

180
Q

What is the name of the product?

A

Lactose

181
Q

What are polysaccharides?

A

> 10 monosaccharides (up to a hundred!)

183
Q

In humans and pigs, where does digestion of carbohydrates begin, and what helps to digest them?

A

Digestion begins in the mouth with alfa-amylase in salivary glands

184
Q

What are major dietary carbohydrates?

A

starch, glycogen, saccharose, lactose

185
Q

After digestion begins in the mouth, how does further digestion occur for carbohydrates?

A
  • Further digestion of carbohydrates is achieved by pancreatic enzymes
  • Digestion is finished by enzymes synthesized by the intestinal mucosa
186
Q

Where does absorption of carbohydrates occur? What is it mediated by and where is that mediator located? What facilitates this action?

A

Absorption of carbohydrates takes place in the duodenum and upper jejunum and is mediated by a Na+-dependent transport mechanism (SGLT1) present at the apical membrane, and by facilitated transport mechanisms present at both the apical (GLUT5) and the basolateral membrane (GLUT2)

187
Q

Where are proteins denatured?

A

In the stomach

188
Q

What partially hydrolyzes protiens in the stomach?

A

Pepsin

189
Q

Where does the final digestion of protiens take place?

A

In the small intestine

190
Q

What are lipids used for?

A

o Prostaglandins

o Steroid hormones

o Phospholipids

o Platelet-activating factor (PAF)

o Sphingomyelin: component of myelin in nerve fibers

191
Q

Fat has amphiphatic character, what does this mean?

A

It has a hydrophillic side and a hydrophobic side of the compound

192
Q

Where does emulsification occur? What is the goal of emulsification?

A

Emulsification occurs in the duodenum and aims to reduce the surface area of the hydrophobic lipid droplets (crucial for lipase function which binds at the interface droplet/aqueous solution)

193
Q

What do bile acids consist of (Chemical composition)?

A

Bile acids (liver) consist of a sterol ring with a side chain of amino acid (taurine or glycin)

194
Q

What are the main dietary lipids?

A

Cholesterol esters, phospholipids, triglycerides

195
Q

Where do lipids digestion start?

A

Partially in the stomach (gastric lipase)

Bile acids emulsify the large fat drops

Emulsified fat droplets are still too large to enter the spaces between microvilli

196
Q

What is the role of pancreatic lipases ?

A

Pancreas lipases hydrolize triglycerides into monoglycerides and free fatty acids

197
Q

What will form mixed micelles?

A

Monoglycerides, FFA, cholesterol, and liposoluble vitamines will form mixed micelles

198
Q

How are mixed micelles absorbed?

A

Mixed micelles approache the brush border membrane of enterocytes where they will be absorbed

199
Q

Do short chain fatty acids form mixed micelles? Why or Why not?

A

Short chain FA do not form mixed micelles (can directly be absorbed)

200
Q

Once absorbed, what is the path of the mixed LCFA?

A

LCFA go into the endoplasmic
reticulum for re-esterification
(re-synthesis) of more complex
lipids as follows:
MAG + free fatty acids —> TAG

201
Q

What is the pathway of chylomicrons?

A

Chylomicrons are released by exocytosis into the lymphatic vessels -> thoracic duct ->
-> left subclavian vein -> blood

202
Q

What are some things that undergo biotransformation in the liver?

A

medicaments, xenobiotics, metabolism
byproducts

203
Q
A

Physiology II (11 decks)

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