Lecture 10: GI physiology Review and Pharmacology Flashcards
1
Q
What is the difference between gallbladder and pancreas anatomy in dogs and cats
A
dogs have pancreatic and common bile duct that stay as separate tubes. The accessory pancreatic duct enter duodenum via minor duodenal papilla and the bile duct entering via the major duodenal papilla
Cats- pancreatic duct and common bile duct both enter duodenum via major duodenal papilla
2
Q
what neurotransmitter does the PNS release into gut and does it promote or stop gut motility
A
ACh- promotes
3
Q
what neurotransmitter does SNS release into gut and does it promote or stop motility
A
NE- stops
4
Q
what neurotransmitters in enteric NS promote gut motility
A
serotonin, motilin
5
Q
what neurotransmitters in the enteric NS stop gut motility
A
dopamine, opioids
6
Q
for serotonin- what is the endogenous source, is it pro or anti motility, what is receptor, and what locations does it affect
A
source: enteric neurons
Pro-motility
Receptor: 5-HT4
Effects entire GI
7
Q
For ACh what is endogenous source, is it pro or anti-motility, receptor and what location does it effect
A
source: enteric neurons- vagus and pelvic neurons
Pro motility
Receptor: Muscarinic ACh
Effects entire GI
8
Q
what is endogenous source of motilin, is it pro or anti motility, what receptor and where does it effect
A
source: intestinal epithelial cells (M cells)
Pro motility
Receptor: Motilin receptor
Effects entire GI
9
Q
is dopamine pro or anti-motility, what receptor and where does it effect
A
anti-motility
D2 receptor
Effects LES, stomach, proximal SI
10
Q
Are opioids pro or anti-motility, what receptor and where in GI does it effect
A
anti-motility
Mu receptors
Effects stomach, SI, LI
11
Q
for epi and NE what is endogenous source, are they pro or anti-motility, what receptors and where do they effect GI
A
source: SNS
Anti-motility
Receptors: alpha2, beta 1 and 2
Effect all smooth muscle sphincters (contraction)n
12
Q
what is metaclopramide used for, what is MOA and site of action
A
pro kinetic- acts on 5-HT4 receptors and dopamine antagonist (D2 receptors)
Acts on pyloric antrum and duodenum
13
Q
what is cisapride used for, MOA, and site of action
A
pro kinetic
Acts on 5-HT4 receptors
Site: LES, pyloric antrum, SI, colon
14
Q
what is erythromycin used for, MOA, and site of action
A
pro kinetic
MOA: motilin analogue
Site: pyloric antrum, SI, colon
15
Q
describe gastric motility
A
- LES, cardia and fundus relax as food enters
- Mixing or constrictor waves- compresses and mixes food in fundus
- Antral peristalsis pushes chyme toward duodenum
- Pyloric sphincter
- Migrating motor complexes (motilin)
16
Q
identify 1-4 in stomach
A
- Gastric pits
- Goblet cells
- Gastric glands
- Chief and parietal cells
17
Q
identify 1-2 in stomach
A
- Parietal cells
- Chief cells
18
Q
what do parietal cells secrete
A
HCl and intrinsic factor
19
Q
what do chief cells secrete
A
pepsinogen
20
Q
what do ECL cells secrete
A
histamine
21
Q
how is pepsinogen activated
A
HCl released—> acidic environment—> activation of pepsinogen to pepsin
22
Q
what is function of pepsin
A
digestion of proteins and collagen
23
Q
what do D cells secrete and what is function
A
somatostatin if pH is too low—> suppresses HCl secretion by parietal cells
24
Q
what do G cells secrete and what are effects
A
gastrin
Gastrin—-> ECL cells—> histamine
Gastrin—> parietal cells—> HCl
25
what are the physiologic roles of gastric acid
1. Activates pepsinogen—> pepsin
2. Frees B12 for absoprtion
3. Duodenal absoprtion of iron, Ca2+
4. Microbiome modulation
5. Pancreatic bicarbonate secretion
26
what are 3 ways to activate partial cells and H+/K+ pump to increase gastric acid
1. G cell—> gastrin—> partial cells—> HCL
2. Vagus nerve—> ACh
3. ECL cell or mast cell—> H2–> histamine
27
what hormones inhibit H/K+ pump and therefore decrease gastric acid
secretin, GIP, VIP, somatostatin, prostaglandins
28
What is MOA of famotidine
H2 receptor blocker
29
what is MOA of omeprazole, esomeprazole, and pantoprazole
proton pump inhibitors
30
PPI or H2 receptors: tolerance with regular administration
h2 receptor blockers
31
which is superior to raising pH, healing: PPI’s or H2 receptor blockers
PPI’s
32
which requires gastric acid to become activated: PPI’s or H2 receptor blockers
PPI’s
33
which reduces acid secretion from any stimulus vs secondary to histamine; PPI or H2 receptor blockers
PPI: any stimulus
H2 receptor blockers: secondary to histamine
34
t or f: PPI’s and H2 receptor blockers are anti-emetics
false
35
PPI’s inhibit __ and might increase effects of other drugs
hepatic cytochrome P450
36
what drug can be used as a coating agent to coat an ulcer
sucralfate
37
sucralfate stimulates __ production in gastric epithelium and decreases __ activity
prostaglandin, pepsin
38
t or f: sucralfate does not need acidic environment to work
false
39
how does co-administration of sucralfate and PPI’s effect efficacy
giving together may reduce efficacy since sucralfate requires acidic environment, and PPI’s will reduce (give sucralfate 30 minutes before PPI)
40
t or f: sucralfate is useful in all parts of GIT
false- won’t reach past upper duodenum
41
what is an adverse effect of sucralfate
constipation
42
use caution and give lower dose of sucralfate in cats with __
CKD
43
What are the functions of SI
1. Chemical digestion
2. Mechanical digestion
3. Absoprtion of mono, diglycerides—> thoracic duct—> R. Atrium
4. Absoprtion of monosaccharides, AA, dipeptides—> portal vein—> liver
5. Secretion and abortion of water and electrolytes
6. Absoprtion of intrinsic factor-B12 complex
7. Tolerance of harmless antigens
44
what occurs in the segmentation contractions of SI
concentration contractions, mixing functions chop the chyme, stops propulsion
45
what mediates segmentation contractions in SI
enkephalinergic neurons (opioids)
46
what mediates peristaltic waves in SI
ENS serotonin
47
what is function of villus in SI
absoprtion
48
what is function of brush border in SI
absorbing and releases digestive enzymes- ;lipase, peptides, sucrase
49
what is function of crypt of SI
Stem Cell production
50
where do enterocytes get their nutrition
lumen (not bloodstream)
51
where are proteins and carbohydrates transferred to after stomach
enter portal vein and travel to liver to get rid of toxins
52
what is responsible for removing fats from SI
lymphatic ducts
53
SI: what indicated by red circle
Peyers patches
54
what is B12 cofactor for
1. RBC synthesis
2. Central and peripheral neurologic processes
55
deficiency in vitamin B12/ cobalamin is due to __ or __ disease
pancreatic or intestinal disease
56
describe what happens to vitamin B12/cobalamin as it travels from stomach to ileum
1. Stomach: cleaved from dietary proteins and bound to R protein
2. Duodenum: released from R protein and binds pancreatic intrinsic factor
3. Ileum: cobalamin/IF complex binds specific receptors for absoprtion
57
what happens to vitamin b12/cobalamin with pancreatic disease
lack of intrinsic factor- needs to be absorbed
58
what happens to vitamin B12/ cobalamin with ileal disease
cobalamin malabsorption
59
what are some functions of LI
1. Reabsorption of water
2. Secretion of bicarbonate, chloride, mucus, potassium
3. Mixing and antiperistaltic contractions to ensure good fecal consistency
4. Gut microbiome interactions
5. Bacterial fermentation of indigestible starches
6. Defecation reflex
7. Tolerance of harmless antigens
60
what is the function of haustrations in colon
contractions that roll and squeeze feces into balls
61
what occurs in defecation reflex
response to feces in rectum, peristalsis of descending colon, contraction of rectum and relaxation of anal sphincters
62
SI or LI
LI- only crypts, no villi
63
what is the function of outer mucus layer of LI
traps bacteria
64
what is function of inner mucus layer in LI
contains IgA and traps bacteria
65
what is cause of malabsoprtive diarrhea
villus atrophy or enterocyte dysfunction
66
what is cause of osmotic diarrhea
presence of osmotically active molecules in the SI lumen that pull in water
67
what is the cause of increased mucosal permeability causing diarrhea
breakdown of normal enterocyte tight junctions and mucous barriers
68
what is the cause of maldigestive diarrhea
lack of pancreatic brush border digestive enzymes
69
what is cause of hyper motility diarrhea
ingesta moves too fast for normal digestion and absorption
70
what is cause of secretory diarrhea
crypt cells stimulated to over secrete water, electrolytes, bicarbonate
71
Laxatives are mainstay treatment for __ and __
constipation and megacolon
72
what mechanism of diarrhea do laxatives cause
osmotic
73
what osmotic laxatives commonly used in small animals
lactulose, miralax
74
How do bulking agents serve as laxatives
irritate colonic mucosa which stimulate secretion of water and mucous into lumen
75
how are stool softeners used as laxatives
salt that decreases surface tension of feces and allows h20 permeation
76
how does docusate work (stool softener)
stimulates enterocyte cAMP—> secretion of H20 and electrolytes
77
why do you not do fleet enemas in cats
contain electrolytes—> hyperphosphatemeia, hyperkalemia
78
What is propectalin, pro-kolin and how do they work
anti-diarrheal
Kaolin- absorb water, bacteria and some toxins
Pectin- absorbs excess water from feces
79
what is loperamide and how does it work
mu-opioid receptor agonist- slows motility and increases sphincter tone throughout GI
80
what is the stimulus for feeding center
ghrelin
81
what is stimulus for satiety center
peptide YY, CCK, insulin, leptin
82
what are the peripheral effects that can disrupt appetite and what is tx
1. Nausea—> anti-emetics
2. Gastroparesis, ileus, constipation—-> pro kinetics
83
what are the central affects that can disrupt appetite
reduced hunger, early satiety
84
what is carpromorelin and what is it used for
ghrelin analog-appetite stimulate
85
what are the averse effects of ghrelin
1. Bad taste—> hypersalivation, nausea, vomiting
2. GI upset
3. Transient bradycardia, hypotension
4. Transient decrease in insulin secretion—> hyperglycemia
86
what is mirtazapine/ mirataz
SSRI’s- appetite stimulant, anti-emetic, pro kinetic effects
87
what are adverse effects of mirtazapine, mirataz
vocalization, agitation, vomiting, tachypnea/tachycardia
88
define vomiting
foreceful, reflex mediated expulsion of GI contents
89
define retching
vomiting against closed LES (unproductive)
90
define regurgitation
passive expulsion of food/fluid from esophagus/pharynx
91
describe the vomiting reflex
1. Peristaltic activity stops
2. Reverse peristalsis moves chyme into duodenum, stomach
3. Duodenum over distended with chyme
4. Stomach, duodenum contract and LES relaxes
5. Glottis closes, diphragm and abdominal muscles contract
6. Forceful expulsion of gastric contents
92
vomiting is initiated by vomiting center in the __
brainstem
93
what are the peripheral stimuli for vomiting reflex
irritation, overdistention, hyperexcitability of GI (related to primary GI dz)
94
what are the central stimuli for vomiting reflex
specific chemicals activating brains CTRZ (outside GI dz)
95
what are the peripheral triggers for vomiting
1. Vestibular system
2. Cerebral cortex
3. GI tract serotonin
4. GI tract stretch
96
what are the central triggers for vomiting
1. Opioids
2. Uremic or hepatoencephalopathic toxins
3. Dopamine (dogs only)
4. Histamine
5. NE
6. NK 1 receptor
7. ACh
8. Serotonin
97
what are the indications to induce vomiting
1. Known or suspected gastric FB
2. Known or suspected recent toxin ingestion
3. <2hrs since ingestion
98
what are the contraindications for inducing vomiting
1. Object is sharp or irritating
2. Intestinal obstruction
3. Patient can’T protect airway (megaesophagus, LP, seizures, obtunded)
99
why is inducing vomiting with hydrogen peroxide not recommended
severe GI irritation, ulceration, severe pneumonia if aspirated
100
what is apomorphine and MOA. Who used in
dopamine receptor agonist, stimulates CRTZ and induces vomiting
Dogs only- cats don’t have DA receptors in CRTZ
101
what is clevor/ropinirole, MOA and who used in
dopamine receptor agonist, stimulates CRTZ and induces vomiting
Used in dogs- not DA receptors in CRTZ of cats
102
what drugs are used to induce vomiting in cats
xylazine, dexmedetomidine
103
what are indications for anti-emetics
1. Acute or chronic vomiting
2. Suspicion of nausea
104
what are contraindications for anti-emetics
1. Concern for FB ingestion
2. Concern for toxin ingestion
105
what is ondansetron and what is MOA
central and peripheral anti-emetic
5-HT3 receptor antagonist in CRTZ and myenteric NS
106
what is maropitant and MOA
central ant-emetic
NK1 receptor antagonist
107
what drug can be used for motion sickness
maropitant
108
what is metoclopramide an what is MOA
central anti-emetic, dopamine receptor antagonist in CRTZ
Also pro kinetic- 5-HT34 agonist
109
t or f: can use metoclopramide as anti-emetic in cats
false- no dopamine receptors in CRTZ
110
what is used as effective reversal of clevor and why
metoclopramdie- since nausea is from dopamine. metoclopramide dopamine antagonist (anti-emetic) and clevor dopamine agonist (induces emesis)
111
how does diphenhydramine and meclizine act as anti-emetics
central ant-emetics
Antagonist H1 receptors in CRTZ
112
how does acepromazine or chlorpromazine act as anti-emetics
central anti-emetics
Dopamine receptor antagonists
113
What are the 3 stimuli for secretion of pancreatic enzymes
1. Acetylcholine
2. Cholecystokinin
3. Secretin
114
what is source of acetylcholine in exocrine pancreas
vagus nerve, nerves of ENS
115
what is source of cholecystokinin (CCK) in exocrine pancreas
duodenal and upper jejunal enteroendocrine cells
116
what is stimulus for release ofCCK
fats and other nutrients in duodenum
117
what is source of secretin in exocrine pancreas
duodenal enteroendocrine cells
118
what os stimulus for secretin
acid and other nutrients in duodenum
119
what fluid secreted from pancreas neutralizes stomach acid
bicarbonate
120
What does exocrine pancreas secrete that allows for ileal b12 absorption
intrinsic factor
121
what does alpha-amylase do in exocrine pancreas
breaks down starches into disaccharides (sucrose, maltose, isomaltase, lactase)
122
what does pancreatic lipase do
breaks down fats into mono and diglycerides
123
what does trypsin do in exocrine pancreas
breakdown proteins to dipeptides, AA
124
what cleaves pro enzymes to enzymes in the pancreas
trypsin
125
bile acids are synthesized by ___ and stored in __
hepatocytes, gallbladder
126
CCK causes ___ and bile acids released into duodenal lumen
gall bladder contraction
127
__forms around small dietary lipid aggregates and solubilizes them
Micelles
128
micelles carry fat globes to ___
enterocyte brush border
129
describe enterohepatic recirculation of bile acids
fats enter duodenum and gallbladder releases bile acids from common vile duct—> travel through intestines and into portal vein—>liver where toxins are removed
130
describe enterohepatic recircuation of bile acids with PSS
fats enter duodenum and travel through intestine—> enter portal vein and then enter shunt that brings some blood back to CVC before going to liver to remove toxins
131
Describe enterohepatic circulation in liver failure
fats enter duodenum and travel and travels through intestine—> portal vein—> liver—> some is stored back in gallbladder and some enters CVC
