Exam # 1 ( GI 1-5) Flashcards
1
Q
What is the GI tract?
A
concentric muscle cylinders lined with an epithelium.
2
Q
What are the accessory organs?
A
Teeth, tongue, salivary glands, liver, pancreas
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.
4
Q
What are identifying characteristics for the ruminant GI tract?
A
fermentation in
the fore stomach system
5
Q
What are identifying characteristics for the equine GI tract?
A
fermentation in the
large intestine. (Small stomach, large intestine is fermentive)
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)
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
8
Q
What is prehension?
A
How food is grabbed.
Species differ in feeding behavior
9
Q
How does prehension occur in Horses?
A
lips (when eating from manger) or incisors (when grazing)
10
Q
How does prehension occur in Cattle?
A
tongue (wrap the tongue around forage) and incisors
11
Q
How does prehension occur in goat and sheep?
A
tongue and lips
12
Q
How does prehension occur in pigs?
A
snout and mandible
13
Q
How does prehension occur in carnivorous animals?
A
canines, incisors, and forelimbs
14
Q
What is mastication?
A
The first act of digestion, involves the actions of the teeth, jaws, tongue, and cheeks
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
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
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
-
18
Q
What kind of meal moves through the GI tract quicker, a hypocaloric meal or a hypercaloric one?
A
Hypocaloric- less to digest
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
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
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)
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
23
Q
What are some disorders of deglutition?
A
Dysphagia which can result from neuromuscular disorder or mechanical obstruction.
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
25
What is the regulatory center for energy homeostasis?
Hypothalamus
26
What is within the hunger center?
Nucl. Paraventricularis, lateral hypothalamus fields, perifornical region
27
What is within the satiety center?
Nucl. ventromedialis
28
What are stimulatory neuropeptides (Hunger) from the hypothalamus?
Neuropeptide Y (NPY) and Orexin
29
What are inhibitory (Satiety) neuropeptides from the hypothalamus?
Melanocyte-stimulating hormone (MSH)
Think of the labradors!
30
What are stimulatory (Hunger) non-hypothalamic hormones?
Ghrelin
31
What are inhibitory (Satiety) non-hypothalamic hormones?
Cholecystokinin (CCK), Peptide YY (PYY), Leptin (fat cells -\> inhibits NPY release and activates MSH release and activity), Insulin (pancreas -\> glucose availability)
32
What are the major salivary glands?
- Parotis (parotid gland)
- Mandibularis (mandibular gland)
- Sublingualis (sublingual gland
33
What are the small salivary glands?
- Ventral jaw glands
- Palate, pharyngeal glands
- Lips glands (labiales)
- Zygomatic glands
34
Which salivary glands provide the largest amount of secretion?
Parotis and Mandibularis account for 90% of salivary secretion
35
What is the primary function of saliva (digestive)?
Protection of the buccal mucosa and teeth
Facilitation of deglutition
Initiation of enzymatic carbohydrate
digestion (human and pigs -\> amylase) -\> pH regulation (HCO -)
36
What are the secondary functions of saliva?
• Immunologic function (Lysozyme, Ig‘s)
• Thermoregulation (panting in dogs)
• Defense mechanism in some species (llamas,
alpacas)
37
What makes up saliva?
99% Water and 1% electrolytes (Na+, K+, Cl-, HCO3-)
38
In the salivary gland, what is produced in the ducts?
Secondary Saliva (K+, and HCO-)
39
In the salivary gland, what is produced in the acinus?
Primary Saliva (Cl-, Na+. H2O)
40
What can be caused by disturbances in saliva production?
- Xerostomia (dry mouth)
- buccal ulcers
- dysphagia
- proliferation of bacterial population
- Cavities
41
What are the four routes secretions of the Gi tract reach their target tissue?
- Endocrine
- Paracrine
- Autocrine (not hormones, does not enter blood)
- Neurocrine
42
What is Neurocrine secretion?
secretions by enteric neurons that affect muscle cells, glands, and blood cells.
43
What is Autocrine secretion?
Secretions of a given cell regulate functions of the same cell.
44
What is paracrine secretion?
Secretions that diffuse through the interstitial space to affect other cells.
45
Where is secretin synthesized?
Duodenum, Jejunum
46
Where is Gastrin Synthesized?
Antrum, Duodenum
47
Where is CCK synthesized?
Duodenum, Jejunum, Ileum
48
Where is GIP synthesized?
Duodenum and Jejunum
49
Where is Motilin synthesized?
Duodenum and Jejunum
50
What is the action of secretin? What is its stimulants?
Stimulates bicarbonate secretion and inhibits acid secretion
Stimulants: Acid, fat, and protein
51
What is the action of Gastrin? What is its stimulants?
Stimulates acid secretion.
Stimulants: Protein, high pH
52
What is the action of CCK? What is its stimulants?
Stimulates pancreatic enzyme secretion and gallbladder contraction.
Stimulants: Fats and proteins
53
What is the action of GIP? What is its stimulants?
Inhibits gastric secretion and stimulates insulin secretion
Stimulants: Fats and glucose
54
What is the action of motilin? What is its stimulants?
Induction of intestinal motility during fasting (MMC)
Stimulants: Acetylcholine
Rest and digest
55
What are the 4 sections of the monogastric stomach?
Cardias, Esophogeal, Fundus and Corpus, Pylorus
56
Which section of the monogastric stomach is larger in horses?
Esophageal
57
Which section of the monogastric stomach is larger in pigs?
Cardia
58
What are the three glandular zones of the stomach? What are their secretions?
Cardias - Mucus
Fundus- HCl, Enzymes
Pylorus- Mucus
59
What are gastric pits?
Gastric folds
60
What do parietal cells secrete and what is their location?
located in the neck of the gastric gland, and secrete HCl and Parietal cells secrete Instrinsic Factor
61
What do chief cells secrete?
secrete proteolytic enzyme precursors such as pepsinogen
62
What are mucus neck cells? What do they secrete?
They are progenitor cells for gastric mucosa. They secrete thin mucus unless they differentiate into one of the other cells. STEM CELLS
63
What is the importance of intrinsic factor secreted by Parietal cells?
Essential for vit. B12 absorption in the ileum
64
What does enteroendocrine cells secrete?
They secrete hormones like Gastrin, GIP, ect
65
Why is HCl important in nature?
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
What are proenzymes?
Proenzymes are are forms enzymes that dont destroy the cells.
67
What does enteroendocrine cells secrete?
G cells - Gastrin
D cells- Somatostatin
I cells- CCK
68
Where do entoendocrine secrete their granule content, and where do they go from there?
They secrete their granule contents into the lamina propria. Some will reach blood capillaries after that.
69
What are mucins?
glycoproteins) are secreted by exocytosis
70
How long do surface mucus cells live?
Surface mucous cells do not live long (regeneration every 3-5 days (↑ mitotic activity in the isthmus of the gastric pit)
71
What are the purpose of mucus cells?
Protection and lubrication of the mucosa.
72
What are the three levels that regulate HCL secretion?
Neural (acetylcholine)
Hormonal (Gastrin)
Paracrine (Histamine
73
What secretes the each of the mediators for HCl secretion regulation?
acetylcholine- vagus nerve
histamine - enterochromatin like cells.
gastrin- vagus nerve
74
At what pH is HCl production inhibited?
\< 3
75
What kind of feedback mechanism is the HCl secretion of parietal cells?
Negative feedback mechanism
76
What is released from D cells that inhibits Gastrin production?
Somatastatin
77
What occurs in the apical membrane after acid secretion?
Canaliculi fuse with the apical (luminal) membrane and vesicles containing H+/K+ ATPase are targeted to the apical membrane increasing HCl secretion
78
What is released from the small intestine when food particles are present?
CCK and Secretin
79
What is the reason that NSAIDS would cause gastric ulcers?
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
TRUE or FALSE: After 3 days on NSAIDS a generally healthy patient is at high risk for a gastric ulcer
FALSE
It would be with long term use of NSAIDs
81
What else does removing COX 1 cause and how can it further worsen gastric ulcers?
Impairs healing via reduced mucosal blood-flow, impaired platelet aggregation and increased bleeding/ injury
82
What else does removing COX 2 cause and how can it further worsen gastric ulcers?
Reduces angiogenesis and reduces leukocyte adherence and increases leukocyte activation which could cause further damage and decrease healing.
83
What is the pH of gastric acid?
(1-4)
84
How does H. Pylori evade being destroyed by the Gastric acid?
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
What is the pH in the proximal part of the stomach in horses and pigs?
4-6
86
Prochymosine is broken down to what? Where? And by who?
In calves and lambs Prochymosine is broken down to chymosine in the abomasum, where hydrolysis of milk protein occurs.
87
Pepsinogen is broken down to what?
Pepsin
88
What can cause gastric ulcers in horses? Why?
\*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
What are the three phases to gastric secretions?
Cephalic
Gastric
Intestinal
90
What occurs during the cephalic phase of digestion?
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
What occurs during the Gastric phase of digestion?
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
What occurs during the Intestinal phase of digestion?
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
What are the three levels of surface convolutions of the small intestine to expand surface area?
Plicae circulares (in some species), Villi, and microvilli.
94
What are the names of the gland like structure at the base of the villi of the small intestine?
crypts of Lieberkühn
95
What is the secretions of paneth cells?
antimicrobial enzymes and peptides
96
What is the function and secretion of mature enterocytes/ absorptive cells?
Function: absorption of nutrients
Secretion: digestive enzymes as well as water, Cl-, and HCO3
97
What are the secretions of Goblet cells?
secretion of mucus
98
What are the secretion of enteroendocrine cells?
hormones such as CCK, secretin, and GIP
99
What are brunners glands? What is their function? What do they Secrete?
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
Where do division and replication of enterocytes occur?
- occurs in the crypts only
Intestinal crypt cells are among the most rapidly regenerating cells of the body
101
What is the turnover time of enterocyte regeneration?
4-7 days
102
What determines the length of the villi in the small intestine?
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
When the proginator cells are differentiated into the needed cell, what occurs? What is the exception?
The cell will migrate up the villi. Paneth cells will migrate down into the crypt and reside between crypt base columnar cells.
104
What is the mediator of water secretion in the small intestine?
All water secretion in the intestine is mediated by osmosis
105
What can cause food to be hyperosmotic and how does the small intestine accomodate for that?
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
As solutes are absorbed in the small intestine, how does water move?
water follows them osmotically back through the epithelium and into the vascular system reaching the blood stream
107
In general what direction does water move in the small intestine?
Water will move in whatever direction to keep the ingesta isoosmotic.
108
What are components/ important information about the large intestine?
- 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
What is a large difference between mucosa within the small intestine and the mucosa of the large intestine?
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
Where do water and nutrients go before entering the vascular system?
Water and nutrients enter first the extracellular fluid
before entering the vascular system
111
What forces are responsible for driving the movement of solutes and water between intravascular and extravascular fluids?
oncotic and hydrostatic forces.
112
How do absorbed nutrients enter the capillaries?
Absorbed nutrients enter then the capillaries by
diffusion from the interstitium (this drives water to the
capillaries too)
113
Where does venous blood from the GI tract collect?
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
TRUE OR FALSE: Lymphatic drainage from the gut passes through the liver and then is reentered into circulation.
FALSE- Lymphatic drainage from the gut bypasses the liver entering the bloodstream through the thoracic duct
115
What can you find in the liver lobule?
Portal venules, arteriole of hepatic artery, bile duct.
116
What kind of capillaries are found in the liver? Why?
Sinusoidal ( this is to allow proteins and large solutes to enter the blood)
117
What are the functions of the liver?
* 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
What are the components the liver produces that is part of the plasma protein?
◦ Albumins
◦ Lipoproteins:
‣ VLDLs
‣ LDLs
‣ HDLs
◦ Glycoproteins: haptoglobin, transferrin
◦ Prothrombin and fibrinogen
◦ Non-immune alfa- and beta-globulins
119
What are VLDLs and what do they do?
Lipoproteins: They transport triglycerides from liver to the other organs.
120
What are LDLs and what do they do?
Lipoproteins: They transport cholesterol esters from liver to the peripheral tissues. (bad cholesterol)
121
What are HDL's and what do they do?
Lipoproteins: They remove cholesterol from the peripheral tissues and transports it to the liver. (good cholesterol)
122
What hormones are synthesized in the liver? What are they?
* Angiotensinogen -\> Prohormone
* Thrombopoetin -\> Hormone (Growth factor)
* IGF (Insulin-like growth factors) -\> IGF 1 and 2
* Hepcidin -\> Small peptide hormone (iron homeostasis)
123
What is biotransformation?
• Group of reactions involved in the conversion of toxic molecules in non-toxic, water soluble and more excretable substances.
124
What is important about most drugs that we can give to patients?
• 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
What is the largest site for biotransformation?
The liver
126
What are the enzymes involved in biotransformation in the liver?
Cytochrome P450 enzymes
127
TRUE or FALSE: Drug Metabolism leads to increased polarity
True
128
What does increased polarity mean in terms of drug metabolism?
makes drugs and their metabolites more water soluble
129
How many phases are involved in biotransformation?
2
130
What occurs in phase one of biotransformation?
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
What occurs in phase two of biotransformation?
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
Where is bile produced?
The bile is produced in the hepatocytes and is modified in epithelial cells of the gallbladder.
133
What is the role of the Gall bladder?
Gallbladder: Storage and concentration through electrolyte and water resorption.
134
What is synthesized to make bile acid?
Bile acids are synthesized from cholesterol and conjugated with amino acids ( glycine, taurine)
135
What is bile acids, and where are they secreted?
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
When bile acids are secreted into the duodenum and emulsify fat droplets in the small intestine, what is formed?
Forming mixed micelles
137
What is the path of bile in the liver?
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
What is the muscle that prevents bile from leaking into the duodenum?
• Sphincter of Oddi (smooth muscle)
139
When there is no digestion, where is bile stored?
gallbladder.
140
What causes oddi's sphincter to relax and release bile?
• 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
What is the refractory mechanism that affects the circulation of bile?
Refectory -\> increased Ach -\> contraction of the smooth muscle.
142
What is the components of bile?
Bile acids, Bile pigment, phospholipids, cholesterine, Na+, K+, Ca++, Cl-, HCO3-
143
What is the pH of bile?
8.2
144
What is the general steps of synthesis and circulation of bile acids?
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
What percentage of bile is made each time we eat? How much is recirculated?
95 % is recirculated, 5% is what is made de novo in the liver.
146
What are the two tissues that compose the pancreas and what do they each secrete?
• 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
What is the exocrine pancreas?
The exocrine pancreas is an acinar gland connected by arborizing system of ducts.
◦ Structure of exocrine pancreas resembles the salivary gland
148
What is the secretion in the acinus of the exocrine pancreas made of?
• Secretion in acinus resembles the primary saliva (i.e Cl- channel apical; Na+/K+/2Cl- cotransporter basolateral);
149
In the exocrine pancreas, where does the addition of HCO3- occur?
In the ducts.
150
What are zygomens?
Inactive forms of proteases which are not going to harm the pancreatic cells.
151
What digestive enzymes are produced in the pancreas?
‣ Peptidases (produced in inactive form): Trypsinogen, chymotrypsinogen, proelastase, procarboxypeptidase A and B.
‣ Nucleases: Ribonuclease, desoxyribonuclease
‣ Amylases: alpha- amylase
‣ Lipases
152
What receptors do pancreatic cells have?
• Pancreatic cells have receptors for acetylcholine, CCK, and secretin
153
How can diet effect the concentration of specific digestive enzymes?
◦ increased starch -----\> Increased amylase
◦ Increased fat and protein ----\> Increased lipases and peptidases.
154
What are the phases of regulation for the exocrine pancreas?
Regulation:
◦ Cephalic phase (site, smell, imagination)
◦ Gastric Phase (dilation of the stomach)
◦ Intestinal Phase
155
What occurs in the intestinal phase of regulation of the exocrine pancreas?
‣ 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
What are two examples of impairment of pancreas secretion?
- Pancreatic insufficiency
- Pancreatitis
157
What is pancreatic insufficiency? What is the clinical signs?
◦ Insufficient production of digestive enzymes by the exocrine pancreas; mal digestion;
◦ Clinical signs: Greasy/oily stools (steatorrhea), polyphagia, rapid weight loss
158
What is pancreatitis? What is the clinical signs?
◦ 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
What does secretin stimulate?
Production of a bicarbonate rich secretion
160
What does acetylcholine and CCK stimulate?
Secretion of an enzyme and chloride rich fluid.
161
What is the active form of trypsinogen?
Trypsin
162
What does it mean to be amphipathic?
One side of compound hydrophilic, one side hydrophobic.
163
When does the reflectory response within the bile duct occur?
can occur just before eating.
164
What is the pathway of bile acids?
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
What causes the conversion of trypsinogen to Trypsin? Where is it activated?
enteropepsidase. In the duodenum
166
During an episode of pancreatitis what occurs to the zymogens that causes local damage of pancreatic cells?
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
What can occur in pancreatitis when trypsinogen, trypsin, and zymogens are prematurely activated?
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
What inflammatory mediators are released during an episode of pancreatitis?
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
What can the release of inflammatory mediators cause in a patient with pancreatitis?
This can lead to shock, disseminated intravascular coagulation (DIC), and death
170
What usually activates zymogens?
They are activated by cleavage of the amino-terminal polypeptide chain. Zymogens are normally not activated until they reach the small intestine.
171
What is the treatment of pancreatitis?
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
What is the prognosis of a patient with pancreatitis? What causes it? Who is more susceptible?
Overweight dogs are more susceptible. There is no known/ definitive cause. Prognosis varies, depending on cause, severity, and chronicity of disease.
173
What are the functions of carbohydrates in the body?
Functions:
- Energy source
- Storage form of energy
- Cell membrane component (communication)
- Structural component (cell wall of bacteria)
174
What are carbohydrates made from?
All carbohydrates are made from monosaccharides
175
Monosacharides are categorized based on what?
Monosaccharides (simple sugars) are categorized according to the number of carbons
177
TRUE OR FALSE: Carbohydrates are the most abundant organic molecules in nature.
TRUE
178
What are disaccharides?
Monosaccharides linked by glycosidic bonds
179
What are oligosaccharides?
3-10 Monosaccharides
180
What is the name of the product?
Lactose
181
What are polysaccharides?
\> 10 monosaccharides (up to a hundred!)
183
In humans and pigs, where does digestion of carbohydrates begin, and what helps to digest them?
Digestion begins in the mouth with alfa-amylase in salivary glands
184
What are major dietary carbohydrates?
starch, glycogen, saccharose, lactose
185
After digestion begins in the mouth, how does further digestion occur for carbohydrates?
- Further digestion of carbohydrates is achieved by pancreatic enzymes
- Digestion is finished by enzymes synthesized by the intestinal mucosa
186
Where does absorption of carbohydrates occur? What is it mediated by and where is that mediator located? What facilitates this action?
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
Where are proteins denatured?
In the stomach
188
What partially hydrolyzes protiens in the stomach?
Pepsin
189
Where does the final digestion of protiens take place?
In the small intestine
190
What are lipids used for?
o Prostaglandins
o Steroid hormones
o Phospholipids
o Platelet-activating factor (PAF)
o Sphingomyelin: component of myelin in nerve fibers
191
Fat has amphiphatic character, what does this mean?
It has a hydrophillic side and a hydrophobic side of the compound
192
Where does emulsification occur? What is the goal of emulsification?
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
What do bile acids consist of (Chemical composition)?
Bile acids (liver) consist of a sterol ring with a side chain of amino acid (taurine or glycin)
194
What are the main dietary lipids?
Cholesterol esters, phospholipids, triglycerides
195
Where do lipids digestion start?
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
What is the role of pancreatic lipases ?
Pancreas lipases hydrolize triglycerides into monoglycerides and free fatty acids
197
What will form mixed micelles?
Monoglycerides, FFA, cholesterol, and liposoluble vitamines will form mixed micelles
198
How are mixed micelles absorbed?
Mixed micelles approache the brush border membrane of enterocytes where they will be absorbed
199
Do short chain fatty acids form mixed micelles? Why or Why not?
Short chain FA do not form mixed micelles (can directly be absorbed)
200
Once absorbed, what is the path of the mixed LCFA?
LCFA go into the endoplasmic
reticulum for re-esterification
(re-synthesis) of more complex
lipids as follows:
MAG + free fatty acids ---\> TAG
201
What is the pathway of chylomicrons?
Chylomicrons are released by exocytosis into the lymphatic vessels -\> thoracic duct -\>
-\> left subclavian vein -\> blood
202
What are some things that undergo biotransformation in the liver?
medicaments, xenobiotics, metabolism
byproducts
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