Gi Physiology

Front 1

what innervates 90% of the gut?

Back 1

craniosacral vagus nerve - parasympathetic

Front 2

what innervates the distal colon?

Back 2

pelvic nerve - parasympathetic

Front 3

the cholinergic response in the gut is [excitatory/inhibitory]

Back 3

excitatory

*increase contractile activity & secretion

Front 4

the adrenergic response in the gut is [excitatory/inhibitory]

Back 4

inhibitory

*decrease contraction & secretion primarily by inhibiting cholinergic nerves

Front 5

what is the enteric nervous system?

Back 5

-extrinsic innervation of gut

- nerves reside in submucosal & myenteric plexus

- secrete variety of mediators

- acted on by para & symp nervous system

- more nerves than in brain!

Front 6

in what species is the functional significance of salivary secretion most important?

Back 6

ruminants & horses

Front 7

what is saliva primarily made of in a ruminant and a non-ruminant?

Back 7

rum: NaHCO3

non: NaCl

Front 8

_____________ modify the primary secretion depending on saliva flow rate

Back 8

ducts

Front 9

T/F - Saliva is impermeable to water

Back 9

kind of false - in the ruminant it can be under the influence of aldosterone if the animals are getting too dehydrated

Front 10

primary stimulation of salivary secretion is [cholinergic/adrenergic] and primary inhibition is [cholinergic/adrenergic]

Back 10

cholinergic - adrenergic

Front 11

4 functions of saliva

Back 11

1. facilitate mastication & deglutition

2. initiate starch & lipid digestion

3. evaporative cooling (panting)

4. enables microbial digestions in reticulorumen

Front 12

cats and dogs lack cutaneous sweat glands - how do they cool themselves?

Back 12

- dead space ventilation

- cats produce copious flow of watery saliva and spread it on their coat for water vaporization

Front 13

how much saliva can ruminants secrete from their parotid duct independent of secretory nerves?

Back 13

100-200 liters/day

Front 14

"hypersecretion of saliva"

Back 14

ptyalism

*most often due to nausea

Front 15

"loss of saliva from moth due to inadequate swallowing most often due to oral pain or dysphagia"

Back 15

pseudoptyalism

Front 16

5 types of salivary gland diseases

Back 16

1. sialoadenitis

2. salivary gland neoplasia

3. sialocele

4. laceration of parotid duct

5. sjogren's syndrome (autoimmune disease)

Front 17

in ruminants, where does the fluid and buffer in the forestomach come from?

Back 17

saliva!

*NO secretory glands in forestomach

Front 18

what parts of the GI system are voluntarily controlled?

Back 18

swallowing & external anal spincter

Front 19

"the act of swallowing"

Back 19

deglutition

Front 20

3 phases of deglutition

Back 20

1. oropharyngeal phase

2. esophageal phase

3. gastroesophageal phase

Front 21

3 stages of oropharyngeal phase of deglutition

Back 21

1. oral stage (prehension, mastication)

2. pharyngeal stage

3. cricopharyngeal stage

Front 22

2 stages of peristalsis & what phase of deglutition they are in

Back 22

primary - initiated via swallowing

secondary - via luminal distension

*esophageal phase

Front 23

which phase of deglutition relaxes the lower esophageal spincter and allows food to pass into the stomach?

Back 23

gastroesophageal phase

Front 24

"difficulty prehending, chewing or swallowing food"

Back 24

dysphagia

Front 25

"the spontaneous and passive expulsion of contents from the esophagus as facilitated by body position and gravity"

Back 25

regurgitation

Front 26

3 major causes of oropharyngeal dysphagia

Back 26

1. oral - failure to prehend or masticate food or form bolus at base of tongue

2. phayrngeal - failure to contract due to neuromuscular weakness or fibrosis

3. circopharyngeal - failure to relax (achalsia) or to contract (chalasia) or does not relax at the right time (dysynchrony)

Front 27

what is the most common type of oropharyngeal dysphagia?

Back 27

dysynchrony in the cricopharngeal region

*does not relax at the right time

Front 28

"foul odor to the breath"

Back 28

halitosis

Front 29

5 functions of esophagus

Back 29

1. eructation (elimination of gases)

2. egestions (birds; elimination of indigestible parts of prey)

3. regurgitation (pathological)

4. rumination (transport for re-mastication)

5. swallowing

Front 30

if the esophagus of a ruminant becomes obstructed, what consequence is likely to kill the animal first?

Back 30

unable to eructate

Front 31

describe muscle content in esophagus for each species

Back 31

dog/ruminant: entirely skeletal muscle

cat/horse/pig - 1st 2/3 is skeletal and terminal portion is smooth

Front 32

in a skeletal muscle esophagus, the [para/symp] nervous system innervates the muscle and secretes what on to which receptors?

Back 32

parasympathetic

acetylcholine

nicotinic

Front 33

what type of epithelial lining does the esophagus have?

Back 33

stratified squamous

Front 34

3 ways to visualize the esophagus

Back 34

1. survey radiographs

- not seen unless there is a problem

2. contrast radiographs w/fluoroscopy

- assess fxn & see radiolucent obstructions

3. endoscopy

- see & fix obstructions; biopsies; NOT fxn!

Front 35

3 most common sites for foreign body obstruction of the esophagus

Back 35

1. thoracic inlet

2. base of heart

3. diaphragm

Front 36

what activates primary and secondary peristalic waves in esophagus?

Back 36

1 - swallowing

2 - local esophageal distension

Front 37

describe innervation of esophageal peristalsis

Back 37

- vagus nerve

- smooth m: vagus secretes Ach onto muscarinic receptors

- skeletal: vagus secretes Ach onto nicotinic receptors

Front 38

what is the upper esophageal spincter?

Back 38

2 pharyngeal muscles that relax only to pass bolus or eructate gas

Front 39

what is the lower esophageal spinchter?

Back 39

*cardia

- physiological spincter

- high pressure zone created by gastric mucosal folds, right crus of diaphragm, enlargement of gastric fundus & positive intra-abdominal pressure

- prevents gastric reflux

Front 40

3 treatments for esophagitis

Back 40

1. feed low-fat diet (promotes gastric emptying)

2. admin promotility drugs that increase lower esophageal spincter tone & promote gastric emptying (metoclopramide or cisapride)

3. proton-pump inhibitor to block gastric acid secretion

Front 41

what is the cardinal sign of esophageal disease?

Back 41

regurgitation

Front 42

3 step diagnostic approach to the problem of regurgitation

Back 42

1. distinguish btwn regurg, vomiting & expectoration

2. rule out medical obstruction

3. rule out motility disorder

Front 43

"expulsion of digesta from the stomach & small intestine"

Back 43

vomiting

Front 44

"reflex contraction of the pharyngeal constrictor muscles that occurs when pharyngeal mucosa is stimulated"

Back 44

gagging

Front 45

"contraction of diaphragm, inspiration against a closed glottis & abdominal contraction; pumping action transfers gastric contents into esophagus"

Back 45

retching

Front 46

"expulsion of fluid or debris from airway; usually associated with cough or harsh forceful expiration"

Back 46

expectoration

Front 47

4 functions of forestomach in ruminants

Back 47

1. provide habitat for microbes

2. mix ingesta with microbial pop to stimulate fermentation

3. retain ingesta until it is appropriate size/consistency

4. remove biproducts of microbial ferm.

Front 48

3 things in the rumen

Back 48

bacteria, fungi & protozoa

Front 49

T/F - the rumen is filled with a collection of microbes that function independently of one another

Back 49

false - one functional organism

Front 50

3 functions of the rumen

Back 50

1. fermentation

2. absorption

3. eructation

Front 51

2 functions of the reticulum

Back 51

1. control of rumen contraction rate

2. retains foreign material

Front 52

parasympathetic innervation of the ruminant GI

Back 52

vagus nerve

Front 53

sympathetic innervation of the ruminant GI

Back 53

splanchnic nerve

*slows or stops forestomach motility

Front 54

how many organisms per mL of fluid are in the rumen?

Back 54

10^12

Front 55

bacteria in the rumen are primarily gram [+/-]

Back 55

negative

*positive increases with grain intake

Front 56

what inhabitant of the rumen is most sensitive to changes?

Back 56

protozoa

Front 57

what is an important function of fungi in the rumen?

Back 57

digestion of otherwise indigestible cell walls

Front 58

3 volatile fatty acids produced by fermentative process in rumen

Back 58

1. acetate

2. proprionate

3. butyrate

Front 59

describe volatile fatty acid acetate in rumen

Back 59

- 60-70%

- forage

- increases methane production

- not removed by liver

- used peripherally to produce ATP

- lipid synthesis

Front 60

describe proprionate in rumen

Back 60

- 20-30%

- grain

- does NOT increase methane production

- completely removed by liver

- used for gluconeogenesis

- lactose production in udder

Front 61

basic equation of rumen fermentation

Back 61

CH2O (carbohydrate) + Protein (or nitrogen) = VFA; CO2; CH4; Microbes (waste products)

Front 62

what is the normal pH of the rumen?

Back 62

5.5

Front 63

what is likely if the pH of the rumen is less than normal?

Back 63

*too much grain

- rapid fermentation = excessive VFA production

- protozoa die & bacteria shifts

> lactobacilli predominate and produce lactic acid, exacerbating rumen acidosis

Front 64

what is likely if the pH of the rumen is higher than normal?

Back 64

*anorexia; poor feed

- anorexia: rumen is small

- poor feed quality: rumen is large & firm

- outflow obstruction: rumen is large & sloshy

Front 65

4 functions of rumen motility

Back 65

1. required to facilitate fermentation

2. allows for rumination

3. move digested food out of rumen

4. remove byproducts (eructation)

Front 66

what is a primary contraction of the rumen?

how often does it occur?

Back 66

mixing

roughly once a minute

Front 67

what is a secondary contraction of the rumen?

Back 67

eructation

Front 68

what innervates the rumen's primary contractions?

Back 68

vagus nerve

Front 69

describe stimulatory innervation of the rumen primary contractions

Back 69

- feeding: buccal receptors of trigeminal nerve

- moderate rumen distension: low threshold receptors in medial wall of reticulum & dorsal sac

Front 70

describe inhibitory innervation of the rumen primary contractions

Back 70

- moderate/severe rumen distention: high threshold receptors in rumen epithelium

- increased VFA conc.: low pH monitored by epithelial receptors

- pain; fever; endotoxemia

Front 71

describe innervation of rumen secondary contractions

Back 71

- rate is autonomous

- stimulation: distension of dorsal sac

- inhibitory

> severe distension; fluid at cardia

> damage to receptors at cardia

> systemic disease

> failure at esophageal transport

Front 72

average times of rumination

Back 72

*depends on coarseness of feed

30-60 min after meal

10-60 min per epidode

up to 7 hours per day

Front 73

describe omasal motility

Back 73

- filter based on particle size

- negative pressure sucks ingesta in

- canal contracts with dorsal sac

- omasal body contracts & forces ingesta into abomasum once it is full

- inhibited by abomasal distension

Front 74

what is the name of the motility disorder of the rumen?

Back 74

vagal indigestion syndrome

*vagus nerve is NOT clinically involved

Front 75

clinical signs of motility disorder of rumen

Back 75

- retention of fluid, feed or gas

- hypermotility

- severe abdominal distension

- hypomotility

Front 76

describe type I vagal indigestion

Back 76

- failure to eructate

- large gas filled rumen

- distension of left flank (apple-shape)

Front 77

describe type II vagal indigestion

Back 77

- failure of rumen/reticulo-omasal outflow

- large fluid-filled rumen

- distension of left flank and ventral right flank (papple)

- rumen pH & chloride are normal

Front 78

describe type III vagal indigestion

Back 78

- failure of abomasal/pyloric outflow

- large fluid filled rumen

- distension of left flank & ventral right flank (papple)

- serum chloride decreased

- serum bicarbonate increased

- rumen pH does not change

Front 79

treatment for each type of vagal indigestions

Back 79

type I & II: left flank exploratory & rumenotomy

type III: right flank exploratory

Front 80

4 functions of the stomach

Back 80

1. storage

2. triturating (grinding down) food

3. controlled delivery rate of food to duodenum

4. acid secretion & regulation

Front 81

6 products that the stomach secretes

Back 81

1. hydrogen ion

2. pepsinogens

3. mucus

4. bicarbonate

5. intrinsic factor

6. water

Front 82

2 hormones that gastric mucosa produces

Back 82

1. gastrin

- stimulates acid & pepsinogen secretion

- regulates mucosal growth

2. somatostatin

- inhibits gastrin release

Front 83

in the cardiac mucosa of the stomach, cardiac glands secrete....

Back 83

mucus & bicarbonate

Front 84

4 types of cells in the proper gastric mucosa and what they secrete

Back 84

1. parietal cells - hydrogen (acid)

2. chief cells - pepsinogen

3. enterochromaffin-like cells (ECL) - histamine

4. D cells - somatostatin

Front 85

2 types of cells in the antral/pyloric mucosa and what they secrete

Back 85

1. G cells - gastrin

2. D cells - somatostatin

Front 86

what type of epithelium does the stomach have?

Back 86

- mostly glandular

- some animals have parts with stratified squamous

Front 87

who has stratified squamous epithelium in their stomach?

Back 87

- man/dog have none

- pig in pars esophagea

- horse above margo plicatus

- cow in reticulorumen

Front 88

what is a major risk regarding the stomach when transporting pigs for slaughter?

Back 88

- when fasted their stomach acid can get to their pas esophageal region, which is stratified squamous and can ulcerate, eventually causing gastric hemorrhage and death

Front 89

3 main receptors of gastric HCL secretion

Back 89

1. G receptors - gastrin

2. H2 receptors - histamine

3. muscarinic receptors - acetylcholine

Front 90

3 stimuli for vagus nerve

Back 90

1. cephalic phase

- thought, taste, physical presence of food in mouth

2. gastric phase

- gastric distension & protein products in lumen

3. intestinal phase

- food in duodenum

Front 91

what is the most important mediator of gastric acid secretion? why?

Back 91

histamine

1. both gastrin & Ach stimulate histamine release from ECL cells

2. cAMP syngergizes with 2nd messenger Ca to stimulate HCl secretion

Front 92

which mediator of gastric acid do we block clinically? with what?

Back 92

H2 blockers

famotidine, cimetidine, ranitidine

Front 93

what are some proton pump inhibitors? when are these typically used?

Back 93

omeprazole; pantoprazole

when there is gastric injury

Front 94

what is the "alkaline tide?" how is it balanced?

Back 94

proton pump generates a transient metabolic alkalosis exchanging H+ & K+

secretion of bicarbonate from pancreas and bile ducts to neutralize gastric acid as it enters the duodenum

Front 95

2 ways that gastric acid secretion is turned off

Back 95

1. stimuli promoting it are no longer active

2. release of somatostatin inhibits gastrin release from G cells and histamine release from ECL cells

Front 96

what protects the gastric mucosa from injury?

Back 96

- gastric mucosal barrier prevents back diffusion of H+

- thick, unstirred layer of mucus adjacent to epitehlium

- trapping of secreted bicarb in mucus gel

- mucosal blood flow

Front 97

4 things that endogenous prostaglandins and nitric oxide do in the stomach

Back 97

1. stimulate mucosal blood flow

2. inhibit cAMP generation by parietal cells

3. stimulate mucus & bicarb secretion

4. cytoprotective

Front 98

what drug is used to treat ulcers?

Back 98

sucralfate (carafate)

- creates an occlusive seal over the ulcer, which prevents back-diffusion of HCl and protects underlying epithelium undergoing repair

Front 99

what drug can be given with NSAIDS to prevent gastric ulceration?

Back 99

misoprostol - cytotec

*synthetic PGE

Front 100

7 causes of GI ulcers

Back 100

1. NSAIDs or corticosteroids

2. fasting/anorexia (large animal only)

3. neoplasia or infiltrative disease

4. foreign body

5. metabolic

6. mast cell tumor (histamine)

7. gastrinoma (gastrin)

Front 101

what is the name for the feces that indicates upper GI bleeding?

Back 101

melena

Front 102

4 major stimuli of vomiting center

Back 102

1. chemoreceptor trigger zone

2. vestibular apparatus

3. abdominal viscera

4. cerebral cortex

Front 103

describe efferent limb of reflex vomit

Back 103

- vagus & sympathetic nerves

- sensation of nausea & salivation

- reverse peristalsis of duodenum moves contents into gastric lumen

- glottis closes: negative intrathoracic pressure

- contraction increases abdominal pressure

- lower esophageal sphincter relaxes - gastric contents move into esophagus (retching)

- rapid expulsion of contents

Front 104

4 metabolic consequences of vomiting

Back 104

1. loss of HCl = metabolic alkalosis

2. loss of HCO3 = metabolic acidosis

3. loss of K+ = hypokalemia

4. loss of H2O = dehydration; hypovolemia

Front 105

describe consequences of "duodenal" vomiting and who does this

Back 105

simple-stomached animals

base > acid = metabolic acidosis

Front 106

describe consequences of "gastric" vomiting and who does this

Back 106

pyloric outflow obstruction; ruminant; human

acid > base = metabolic alkalosis

Front 107

if a dog has a metabolic alkalosis after vomiting, what should you suspect?

Back 107

pyloric outflow obstruction

Front 108

3 steps in diagnostic approach to vomiting in small animals

Back 108

1. confirm vomiting vs. regurg/expectoration

2. rule out extra-GI causes

3. rules out GI causes

Front 109

3 things that stimulate gastrin release

Back 109

1. gastric distension

2. protein products in gastric lumen

3. vagal stimulation

Front 110

in response to feeding, gastric motility is stimulated by......

Back 110

gastrin

Front 111

4 parts of the stomach and their function

Back 111

1. fundus - receives & stores ingesta & adapts to increases in volume

2. body - mixes saliva & gastric juices w/food

3. antrum - regulates propulsion of food past pyloric sphincter into duodenum

4. pylorus - allows small amounts of finely ground liquid to pass into duodenum

Front 112

what 2 things are secreted to inhibit gastric motility?

Back 112

1. secretin - in response to high acidity

2. CCK - lipid entering proximal duodenum

Front 113

"vomiting blood"

Back 113

hematemesis

Front 114

"bleeding from the colon" (fresh blood on feces)

Back 114

hematochezia

Front 115

describe location of pancreatic and common bile duct openings in dog vs cat

Back 115

dog: next to one another

cat: common duct, causing more clinical issues

Front 116

what is "triaditis?"

Back 116

concurrent inflammation of intestine, pancreas and biliary tract of cats since they share a common duct into the duodenum

Front 117

4 endocrine cells in pancreas and what they secrete

Back 117

1. alpha cells = glucagon

2. beta cells = insulin

3. delta cells = somatostatin

4. F (PP) cells = pancreatic polypeptide

Front 118

general overview of the exocrine function of pancreas

Back 118

digestive enzymes synthesized and secreted as inactive precursors to prevent pancreatic auto-digestion

Front 119

4 main categories of proteins secreted by pancreas

Back 119

1. proteolytic enzymes

2. lipolytic ezymes

3. amylolitic enzymes

4. nucleases

Front 120

4 most important zymogens secreted by pancreas

Back 120

1. trypsinogen

2. lipase

3. alpha-amylase

4. trypsin inhibitor

Front 121

once in the lumen of the small intestine, zymogens are activated by the proteolytic enzyme, _____________ which resides ___________

Back 121

enteropeptidase

epithelial brush border of duodenum

Front 122

what 2 things are required to activate pancreatic digestive enzymes?

Back 122

1. brush border enterokinase

2. luminal trypsin

Front 123

4 reasons why the pancreas does not digest itself

Back 123

1. enzymes that attack membranes are synthesized as inactive zymogens and enzymes secreted in active forms do not attack membranes

2. enzymes secreted in membrane-bound compartments

3. pancreas contains intracellular trypsin inhibitor

4. activating enzyme is separate from pancreas

Front 124

what are the 2 main disease of the pancreas?

Back 124

1. pancreatitis

2. exocrine pancreas insufficiency (EPI)

Front 125

which breed is associated with EPI?

Back 125

german shepards

Front 126

how can you diagnose EPI?

Back 126

blood test: trypsinogen-like immunoreactivity (TLI)

- with EPI there will be no trypsinogen in the blood

Front 127

EPI results in....

Back 127

- nutrient maldigestions

- weight loss

- osmotic diarrhea

- small intestine bacterial overgrowth

Front 128

"fat diarrhea"

Back 128

steatorrhea

Front 129

3 phases of pancreatic secretion

Back 129

1. cephalic phase

2. gastric phase

3. intestinal phase

*all mediated via vagus nerve

Front 130

what does secretin secretion do in pancreas?

Back 130

bicarbonate-rich fluid from pancreatic duct epithelium

Front 131

what does CCK secretion do in pancreas?

Back 131

enzyme secretion from acini

Front 132

3 functions of bicarbonate-rich fluid secreted from pancreas

Back 132

1. neutralizes gastric acid entering duodenum

2. provides optimal pH for pancreatic & brush border enzymes to function

3. increases solubility of bile acids & fatty acids

Front 133

3 causes of cobalamin (B12) deficiency

Back 133

1. exocrine pancreatic insufficency (cats)

2. small intestinal bacterial overgrowth

3. malabsorptive disease of ileum

Front 134

where is intrinsic factor secreted?

Back 134

dogs: parietal cells of stomach & pancreas

cats: pancreas only

Front 135

describe absorption of B12

Back 135

- ingested in diet

- recieved and bound by intrinsic factor

- receptors in ileum bind complexes ONLY

- absorbed in bloodstream

*B12 is responsible for cell proliferation

Front 136

what happens in cats (re: B12) with EPI?

Back 136

- exacerbates diarrhea

- intestinal crypt stem cells proliferate slowly without B12

- villus atrophy & poor surface digestion

Front 137

if you remove the pancreas on a cat, what disease are you left with and how to treat them?

Back 137

1. diabetes mellitus - insulin

2. EPI - enzyme supplements

3. B12 deficiency - injectible B12

Front 138

what is the key function of the liver in GI physiology?

Back 138

synthesis of bile acids

Front 139

describe blood supply to the kidney

Back 139

- hepatic artery (20%) & portal vein (80%)

- portal venous circulation is 2nd in series of 2 capillary beds

Front 140

3 functions of the portal vein in the liver

Back 140

1. process GI nutrients

2. growth factors for liver

3. removal of GI toxins

Front 141

what disease do you get when you have a congenital portosystemic vascular shunt?

Back 141

hepatic encephalopathy

*yorkies & maltese

Front 142

treatments for hepatic encephalopathy

Back 142

1. low protein diet (reduces NH3 formation)

2. antibiotics (reduce bacterial metabolism of protein to NH3)

3. lactulose (increase transit of food and trap NH3 as NH4+

4. treat concurrent problems (GI bleeding)

5. surgical ligation of shunt vessel

Front 143

clinical signs of hepatic encepalopathy

Back 143

salivation, seizures, head pressing, vomiting

Front 144

describe differences between congenital and acquired portosystemic shunts

Back 144

congenital: single shunt; <1 year old; no ascites; surgically correctable

acquired: multiple shunts; >4 years old; ascites present; not surgically correctable

Front 145

3 functions of bile

Back 145

1. provides bile acids for fat assimilation

2. excretory route for fat-soluble substances

*failure to excrete bilirubin results in jaundice

3. contains electrolytes, water, mucus, IgA, etc.

Front 146

"functional product of bile that is needed for fat assimilation"

Back 146

bile acids

Front 147

"waste product of hemoproteins that is excreted by liver into bile"

Back 147

bilirubin

Front 148

5 causes of icterus

Back 148

1. pre-hepatic: increased hemolysis of RBC

2. hepatic: stasis of bile within liver

3. post-hepatic: obstruction of bile duct

4. sepsis

5. anorexia - horses only*

Front 149

"white poop" - what causes that?

Back 149

acholic feces ("angel poop")

- 100% obstruction of bile duct

Front 150

2 primary bile acids

Back 150

1. cholic acid

2. chenodeoxycholic acide

Front 151

what are the primary bile acids synthesized from?

what is the rate limiting step?

Back 151

cholesterol

7-alpha-hydroxylation

Front 152

after they are synthesized, the primary bile acids are conjugated with what in cat vs. dog?

Back 152

cat/dog: taurine

dog: glycine

Front 153

what happens if a cat has a taurine deficiency?

Back 153

- dilated cardiomyopathy

- central retinal degeneration

*rare unless cat is eating only dog food

Front 154

conjugated bile acids are actively transported from the hepatocyte to the ______________

Back 154

canlicular bile

Front 155

significant diseases of the gallbladder

Back 155

- bacterial infection

- rupture

- obstruction

- mucocele formation

*stones are rare in domestic species

Front 156

what does ursodiol do?

Back 156

- synthetic bile originally from black bears

- very hydrophilic

- increases circulation of bile acid pool

- over time, replaces hydrophobic bile acids

Front 157

CCK's role in gallbadder

Back 157

- released from proximal intestine in response to intraluminal fat

- results in gallbladder contraction & spincter of Oddi relaxation with discharge of bile into lumen of proximal duodenum

Front 158

secretin's role in gallbladder

Back 158

- released from proximal intestine in response to intraluminal fat

- stimulates bicarb secretion by ducts & aids pancreatic secretions in neutralization of gastric acid

Front 159

describe bile acid movement in ileum with %'s

Back 159

95% - reabsobed into portal vein and reused

5% - lost in feces

(must be replaced with synthesis of new bile acids)

Front 160

the entire bile acid pool recirculates approximately ____________ for every meal

Back 160

twice

Front 161

in a bile acid test, the presence of bile either when fasted or after a meal should be.....

Back 161

low for working liver

Front 162

describe triglyceride movement through digestions

Back 162

1. lipase separates into FA & BMG

2. FA joins with bile salts -> spherical micelle

3. micelle travels to brush border of intestine where bile salts break off to go do it again

4. FA & BMG packaged in spherical chylomicrons

5. travel via lymph to heart/systemic circulation

Front 163

clinical approach to evaluation of the liver

Back 163

1. screening test (serum biochem panel)

2. function test (bile acid)

3. liver imaging (ultrasound)

4. liver biopsy

Front 164

"progressive disease of the liver characterized by diffuse damage to hepatic parenchumal cells, with nodular regeneration, fibrosis & disturbance of normal architecture"

Back 164

cirrhosis

Front 165

"abnormal accumulation of serous fluid in peritoneal cavity"

Back 165

ascites

Front 166

major site of nutrient digestion and absorption

Back 166

small intestine

Front 167

3 methods for lumen digestion

Back 167

1. pancreatic amylase

2. pancreatic protease

3. pancreatic lipase & bile acids

Front 168

2 methods for surface digestion

Back 168

1. brush border disaccharides

2. brush border peptidases

Front 169

T/F: every nutrient absorbed in the small intestine has a specific transporter

Back 169

true

Front 170

5 major cell types of the small intestinal villous mucosa

Back 170

1. columnar absorptive cells
2. mucous (goblet) cells
3. intraepithelial lymphocytes
4. enterochromaffin cells
5. undifferentiated cells

Front 171

undifferentiated cells are located in the _________ and differentiated cells are located in the _____________

Back 171

crypts

villous

Front 172

how long is the turnover rate of tissue from crypt to villus top?

Back 172

2-4 days

Front 173

what kind of epithelium does the small intestine have?

Back 173

simple columnar epithelium

Front 174

the villus is for [absorption/secretion] and the crypt is for [absorption/secretion]

Back 174

absorption

secretion

Front 175

the normal net balance of secretion/absorption is in favor of....

Back 175

absorption

Front 176

is it worse to have a disease that targets the villus or the crypts?

Back 176

crypts - you can regrow your villus if you still have active crypts

Front 177

3 simple monosaccharides

Back 177

1. glucose

2. fructose

3. galactose

Front 178

disaccharides - what are they and how do we absorb them?

Back 178

- sucrose & lactose

- split by enzymes expressed in brush border membrane of villous epithelium

Front 179

polysaccharides - what are they and how do we absorb them?

Back 179

- starch, glycogen, fiber
- first broken down into short linkages of glucose by amylase secreted by pancreas
- linkages broken down by glucose monomors by brush border enzymes

Front 180

is fiber digestible by mammalian enzymes?

Back 180

nope - they have a beta-1-4 link; we need an alpha link

Front 181

3 characteristics of oral rehydration solutions

Back 181

1. does not provide significant nutrition

2. requires functional villus epithelial cells

3. does not stop D+ but increases net water absorption

Front 182

3 stages of protein digestion & absorption

Back 182

1. intraluminal digestion (proteolytic enzymes secreted by pancreas)
2. surface digestion (brush border peptidases)
3. intracellular digestion

Front 183

4 stages of lipid digestion

Back 183

1. lipolysis in pancreas
2. micellar solubilization with bile acid in liver
3. absorption in jejunal mucosa
4. delivery to lymphatics

Front 184

3 functions of the colon

Back 184

1. microbial fermentation

2. reabsorption of electrolytes & water

3. storage

Front 185

species have similar ____________ of short chain fatty acids in their colon but different __________

Back 185

concentrations

capacity for synthesis

Front 186

where is the pacemaker of the colon?

Back 186

transverse colon or pelvic flexure

Front 187

soluble ingesta usually reaches the cecum how long after ingestion?

Back 187

2 hours

Front 188

how often does the cecum empty?

Back 188

every 3-4 minutes

Front 189

why is there an antiperistaltic contraction in the ventral colon?

Back 189

resists flow of ingesta and allows for longer storage

Front 190

how long does most particulate matter take to pass through large colon?

Back 190

1-4 days

Front 191

where is most of the water absorbed from the GI tract?

Back 191

small intestine

Front 192

where is water absorbed most efficiently?

Back 192

colon

Front 193

describe water absorption in the proximal colon

Back 193

- surface epithelium absorbs NaCl & water
***no nutrient transporters

- crypt epithelium secretes NaCL & water

Front 194

describe water absorption in the distal colon

Back 194

- both crypt and surface epithelium absorbs NaCL and water under control of aldosterone
***no nutrient transporters

Front 195

in horses, there is a net ___________ of water moving in the ascending colon and a net ________ in the descending colon

Back 195

balance

reabsorption

Front 196

SCFA [inhibit/stimulate] mucosal prostaglandins, which [inhibit/stimulate] net water absorption

Back 196

stimulate

inhibit

Front 197

diagnostic approach to problem of chronic D+

Back 197

1. determine if large or small bowel D+

2. rule out extra-GI causes

3. rule out GI causes

Front 198

when ruling out GI causes of small bowel D+, what order do you do tests?

Back 198

1. maldigestion - TLI test

2. malabsorption - everything else

Front 199

characteristics of small bowel D+

Back 199

- increased appetite (unless systemically ill)

- weight loss

- large volume of feces with normal frequency

Front 200

characteristics of large bowel D+

Back 200

- normal appetite

- no weight loss

- increased frequency & +/- blood/mucus

Front 201

"an increase in fluidity, volume and/or frequency of bowel movements"

Back 201

diarrhea

Front 202

"a more encompassing term that refers to maldigestion and/or malabsorption of food substances"

Back 202

malassimilation

Front 203

"failure to primarily digest food substances"

Back 203

maldigestion

Front 204

"failure to primarily absorb food substances"

Back 204

malabsorption

Front 205

"any disease process that leads to increased gut permeability and the enteric loss of plasma proteins"

Back 205

protein losing enteropathy (PLE)

Front 206

"greasy, grey appearing stool due to the presences of malabsorbed fat"

Back 206

steatorrhea

Front 207

"painful or difficult defecation"

Back 207

dyschezia

Front 208

"fresh blood within or coating the stool"

Back 208

hematochezia

Front 209

"ineffectual or painful straining to defecate"

Back 209

tenesmus

Front 210

4 main mechanisms of D+

Back 210

1. osmotic

2. secretory

3. permeability

4. motility