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Veterinary Physiology > Gastrointestinal Physiology > Flashcards

Gastrointestinal Physiology Flashcards

1
Q

Intrinsic regulation involves (2) and is responsible for

A

local nervous and endocrine systems; specific GI functions

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2
Q

Extrinsic regulation involves (3) and is responsible for

A

CNS, ANS, endocrine system; broad promotion or inhibition of GIT activity

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3
Q

the myenteric plexus controls ________ and gets its sensory info from _________

A

motility; mechanoreceptors

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4
Q

the submucosal plexus controls _______ and gets its sensory info from __________ in ________

A

secretions; chemoreceptors; mucosa

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5
Q

What coordinates motor and secretory activity in the GIT

A

interneurons (between myenteric and submucosal plexus)

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6
Q

describe nerve endings in the ENS

A

no synapse; NT is released diffusely within tissue; motor axons end in varicosities

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7
Q

varicosities release _________, which are (2)

A

neurocrines; NTs or hormones

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8
Q

what enteric NTs are excitatory

A

acetylcholine, tachykinins (substance P)

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9
Q

substance P is involved in (2)

A

pain; vomiting (via CTZ in medulla)

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10
Q

what enteric NT peptides are inhibitory

A

somatostatin; NE/E; PACAP

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11
Q

what enteric NT non-peptides are inhibitory

A

NO, ATP

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12
Q

what enteric NT is inhibitory to muscle but stimulatory to glands

A

VIP (vasoactive intestinal peptide)

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13
Q

most of the GI tract is supplied by what nerve

A

vagus

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14
Q

the pelvic nerve supplies

A

descending colon and rectum (and bladder)

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15
Q

the vagus nerve uses what NT

A

ACh (stimulatory to gut muscle and secretions; vasodilates; relaxes sphincters)

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16
Q

sympathetic afferent nerves synapse in (2) ganglions

A

celiac and mesenteric

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17
Q

splanchnic nerves release what NT

A

NE (inhibits motility and secretions; contracts sphincters; vasoconstricts)

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18
Q

_________ afferent nerves (which are _________) mediate normal gut function, whereas ___________ afferent nerves (which are ___________) signal pathological conditions

A

vagal, parasympathetic; splanchnic, sympathetic

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19
Q

where is information from visceral afferents integrated

A

brainstem mainly

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20
Q

most GI functions are (conscious or subconscious)

A

sunconscious

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21
Q

T/F GI functions are completely subsconscious

A

F

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22
Q

intrinsic gut hormones are mainly _________ released from ________ cells

A

peptides; enteroendocrine

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23
Q

T/F enteroendocrine cells look alike because they each secrete multiple hormones

A

F; they look alike but each secretes a single hormone

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24
Q

enteroendocrine cells have what effects

A

autocrine, paracrine and endocrine

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25
Q

how are some GI hormones involved in cancers

A

some promote mucosal growth

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26
Q

cytokines released by the mucosal immune system affect gut (2)

A

mucosal immune system; motility and secretions

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27
Q

T/F the GIT is predominantly self-regulated by intrinsic nerves and hormones

A

T

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28
Q

what is transit time

A

time taken by food to travel from one gut location to another

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29
Q

what are the 4(5) functions of the GI tract and examples of each

A
  1. propel ingesta (peristalsis)
  2. retain ingesta (sphincter contraction)
  3. break up and mix ingesta (segmentation)
  4. circulate ingesta (segmentation)
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30
Q

T/F GI smooth muscle contains gap junctions to electrically couple the cells

A

T

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31
Q

what are the pacemaker cells of the GI smooth muscle

A

Interstitial Cells of Cajal (ICCs)

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32
Q

what are slow waves

A

ICCs intrinsically, rhythmically depolarize (and then repolarize)

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33
Q

T/F slow waves cause firing of APs and contraction

A

F; the waves are of subthreshold depolarization

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34
Q

when does contraction of GI muscle occurs

A

when slow waves coincide with excitatory NT release

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35
Q

slow waves determine _________ whereas NTs determine ___________

A

pattern of contraction; whether the contraction occurs or not

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36
Q

waves travel in what direction along GI smooth muscle

A

aborally

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37
Q

contractions in the proximal stomach are _________ whereas those in the antrum are __________

A

weak; strong

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38
Q

the peristaltic reflex is entirely _________

A

internal to the ENS

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39
Q

distention of a food bolus ____________ circular muscle proximally and ____________ circular muscle distally

A

stimulates (Ach, substance P); relaxes (ATP, NO, NE, VIP)

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40
Q

mouth/pharynx/larynx is controlled by ________, esophagus in ruminants/dogs is controlled by ________, esophagus in cats and horses is controlled by _________ and the stomach and intestines are controlled by ________

A

CNS; ANS; ANS/ENS (cranial vagus, caudal ANS/ENS); ENS

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41
Q

prehension means

A

grasping food

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42
Q

prehension is controlled by ________ muscles and involves cranial nerves (3)

A

skeletal; facial, glossopharyngeal, trigeminal

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43
Q

what can cause issues with mastication

A

poor dentition and gum disease

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44
Q

the voluntary stage of deglutition involves _________; the involuntary stage of deglutition involves __________ and cranial nerves

A

movement of the bolus into the oropharynx by the tongue; movement of the bolus from the oropharynx to the esophagus; cranial nerves 5, 7, 9, 10, 12

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45
Q

the upper esophageal sphincter is called the

A

cricopharyngeal sphincter

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46
Q

what is an important roleof the cricopharyngeal sphincter that prevents colic

A

prevents swallowing of air, which can cause colic

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47
Q

what propels food from pharynx to stomach; what muscle type and nerves are involved

A

peristalsis in the esophagus; striated mostly; vagus

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48
Q

T/F with fragmentation,there is net forward movement

A

F

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49
Q

functions of saliva (5)

A

lubricates; digests (amylase and lipase); antibacterial (lysozyme); grooming; thermoregulation

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50
Q

salivation is stimulated by ________ (what molecule) and inhibited by ________ (what molecule)

the facial nerves that control salivation are (2)

A

Ach (released by glossopharyngeal and facial); NE/E

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51
Q

two broad categories that stimulate salivation

A

ANS (and CNS) and natural stimuli

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52
Q

acini in salivary glands secrete (4)

A

mucus, enzymes, electrolytes (Na, Cl), water

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53
Q

when dehydrated, aldosterone stimulates _________ (2) to be reabsorbed in the salivary gland and _________ (2) to be secreted; this makes the saliva (2)

A

Na/Cl reabsorbed; K/HCO3 secreted; saliva becomes hypotonic and neutral to alkaline

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54
Q

parotid salivary glands primarily have ________ secretion

A

serous

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55
Q

ruminant saliva characteristics

A

voluminous, alkaline, high in Na and HCO3; helps buffer rumen contents

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56
Q

roles of the stomach (4)

A

stores food, breaks down food, starts digestion (HCl and proteolytic enzymes), released chyme

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57
Q

stomach movements are controlled by (3)

A

ANS, ENS, gut hormones

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58
Q

the _________ of the stomach is responsible for storage

A

proximal part (antrum and most of body)

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59
Q

the _______ of the stomach is responsible for churning and mixing

A

antrum

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60
Q

as food enters, the proximal stomach ______ due to ________ innervation

A

relaxes; vagus

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61
Q

T/F salivary enzymes can digest food throughout the entire stomach

A

F; only in the proximal stomach

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62
Q

stomach motility is controlled by (2)

A

ENS and vagus (PSNS)

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63
Q

what controls that only small particles can leave the pylorus

A

significant smooth muscle tone in the pylorus

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64
Q

gastric emptying is promoted by ______________ factors and inhibited by ________________ factors

A

gastric factors (secretion of gastrin due to stretch and composition of food); duodenal factors (that reflect newly arrived bolus such as low pH, high osmolarity)

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65
Q

once chyme enters the duodenum, it inhibits further emptying of the stomach by stimulating (3)

A

Afferent neurons in vagus -> decrease vagal tone/increase sympathetic tone

Afferent ENS cells

Secretion of cholecystokinin and somatostatin (from duodenal enteroendocrine cells)

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66
Q

what is the migrating motor complex? when does it occur

A

occurs between meals; pylorus relaxes and a strong wave of peristalsis sweeps the antrum, forcing less digestible food out en masse to the duodenum and colon

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67
Q

cyclical release of ______ from the ____ stimulates the migrating motor complex

A

cyclical release of motilin from the SI (stimulated by ACh)

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68
Q

during vomiting, intercostal and abdominal muscles __________ whereas stomach muscles _______

A

contract; relax

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69
Q

the pH of vomited food is _________ and comes from the ________ stomach whereas the pH of regurgitated food is _________ and comes from the _______ stomach

A

<5; distal; >7; proximal

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70
Q

The cardiac glands consist of

A

mucous cells

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71
Q

The fundic glands consist of

A

mucous cells, parietal cells, chief cells, enteroendocrine cells, mast cells

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72
Q

The pyloric glands consist of

A

mucous cells, a few G cells, a few parietal cells

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73
Q

surface mucous cells in all areas of the stomach secrete

A

neutral to alkaline mucous

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74
Q

parietal cells secrete (2)

A

HCl and intrinsic factor

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75
Q

chief cells secrete

A

zymogens

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76
Q

parietal cells contain receptors for (6)

A

ACh (+), histamine (+), gastrin (+), CCK (+), somatostatin (-), secretin (-)

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77
Q

what is the best method to inhibit gastric acid secretion by parietal cells

A

proton pump inhibitors; eventually H+ concentration rises high enough that CA catalyzes the reverse reaction

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78
Q

T/F we manipulate transport of Cl to the lumen as a way to inhibit gastric acid production

A

F; we only manipulate H+ secretion

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79
Q

Chief cells secrete _______________ zymogens, which are cleaved by ______________ into ______ enzymes that digest ___________

A

inactive (pro-enzyme); HCl; active; proteins

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80
Q

In monogastric animals the inactive zymogen is ____________ which becomes __________ once activated by HCl

A

pepsinogen; pepsin

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81
Q

In ruminants the inactive zymogen is ___________ which becomes __________ once activated by HCl

A

prochymosin; chymosin

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82
Q

chymosin is found in the __________ of ruminants

A

abomasum

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83
Q

what does chymosin do in ruminants

A

digests kappa-casein, which curdles the milk, slowing transit time and allowing better digestion in young ruminants

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84
Q

what is the role of mast cells in the stomach

A

secrete histamine, which acts via H2 receptors on parietal cells to stimulate HCl secretion

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85
Q

what is the stimulus/signal for g cells to release gastrin

A

peptides, amino acids and calcium in the stomach lumen

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86
Q

gastrin stimulates (2)

A

HCl secretion from parietal cells directly; histamine release from mast cells (which indirectly causes parietal cells to secrete HCl)

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87
Q

During the cephalic (anticipation) phase of HCl secretion, release of _______ from ________ stimulates _______ receptors on ________ and _________ cells, which overall acts to ________ HCl secretion

A

ACh; vagus; muscarinic; parietal; G-cells; increase

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88
Q

During the gastric phase of HCl secretion, ______________ and ____________ trigger ______ release of _____; food in the stomach raises pH, which further stimulates __________

A

chemoreceptors and stomach distension; ENS; ACh (stimulates parietal directly and gastrin secretion); further increases gastrin secretion

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89
Q

what inhibits HCl secretion

A
  1. low pH inhibits gastrin secretion (which reduces parietal HCl secretion)
  2. chyme in duodenum triggers release of somatostatin (inhibits parietal HCl secretion) and secretin (stimulates somatostatin and PGE2, also triggers bicarb release)
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90
Q

the endocrine pancreas is responsible for __________ and the exocrine pancreas is responsible for ___________

A

regulation of blood glucose; secretion of digestive enzymes

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91
Q

pancreatic enzymes function best in what environment

A

neutral to alkaline

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92
Q

what pancreatic cells secrete HCO3 and H2O

A

centroacinar and duct

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93
Q

what is an indigestible carbohydrate

A

cellulose

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94
Q

most enzymatic digestion occurs by

A

hydrolysis (for lipids, carbs and proteins)

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95
Q

lipase hydrolyzes____ into ____ and requires

A

neutral lipids into fatty acids and monoglycerides; co-lipase

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96
Q

cholesterol esterase hydrolyzes

A

cholesterol esters

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97
Q

phospholipase function

A

splits fatty acids from phospholipids

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98
Q

pancreatic zymogens include

A

trypsinogen -> trypsin, chymotrypsinogen -> chymotrypsin; proelastase -> elastase; procarboxypolypeptidases -> carboxypeptidase

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99
Q

what activates intestinal zymogens

A

mainly trypsin

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100
Q

why doesn’t the pancreas digest itself (1)

A

secretes inactive zymogens; trypsin inhibitors released alongside zymogens (gets diluted in intestinal lumen)

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101
Q

when does EPI usually occur

A

secondary to chronic pancreatitis

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102
Q

pancreatic cells have receptors for

A

ACh (enzymes and HCO3), gastrin (enzymes), CCK (enzymes), secretin (HCO3)

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103
Q

decreased pH in the duodenum stimulates the release of

A

secretin (secretes HCO3)

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104
Q

increased peptides and fat in the duodenum stimulates

A

CCK secretion (gallbladder contraction and release of pancreatic enzymes)

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105
Q

proteins and Ca in the pylorus stimulates

A

gastrin release, which acts on parietal cells/M cells AND stimulates the release of pancreatic enzymes

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106
Q

what provides negative feedback on pancreatic enzyme/HCO3 secretion

A

rise in duodenal luminal pH; chyme digestion/absorption

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107
Q

what does splanchnic circulation supply

A

stomach, small intestines, colon, pancreas, liver, spleen

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108
Q

T/F the splanchnic circulation has some degree of autoregulation

A

T

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109
Q

approx 75% of blood flow in GIT is to

A

mucosa

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110
Q

two main molecules that increase bloodflow to the GIT are

A

prostaglandins and ACh

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111
Q

two main molecules that decrease bloowflow to the GIT are

A

NE and PGF

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112
Q

nutrient absorption and increased metabolic _______ bloodflow to the GIT

A

increase

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113
Q

gastric ulcers can be caused by

A

chemicals, pathogens, decreased gastric bloodflow (ex. inhibition of prostaglandins by NSAIDs and glucocorticoids)

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114
Q

villi are very sensitive to ________ because of __________

A

hypoxia (end-organs); countercurrent O2 exchange

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115
Q

mild ischemia causes _____________, moderate ischemia causes _________ and severe ischemia causes __________

A

diarrhea; ulceration and bleeding; perforation and peritonitis

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116
Q

why does decreased bloodflow lead to ulcers

A

HCO3 production and mucus production relies on water, which comes from blood supply

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117
Q

the 2 roles of bile are

A

lipid digestion and waste elimination

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118
Q

bile salts, which are made from _______________, act like __________ to ___________lipid droplets

A

cholesterol; detergents; disperse

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119
Q

in hepatocytes, bile acids are _____________, which ______________

A

conjugated to amino acids; inhibits reabsorption from the biliary tract and duodenum

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120
Q

bile acids are ____________ transported into hepatic canaliculi

A

actively

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121
Q

purpose of the gallbladder

A

stores and concentrates bile

122
Q

gallstones are commonly formed from

A

calcium carbonate; bilirubin salts

123
Q

what is the stimulus for release of bile acids

A

fat in the duodenum triggers release of CCK from enteroendocrine cells

124
Q

CCK ___________ the gallbladder sphincter and______________ gallbladder smooth muscle

A

relaxes; contracts

125
Q

bile acids act like _______________, by _____________ surface tension at the fat globule surface

A

detergents; decreasing

126
Q

after triglycerides are broken down into FFA and monoglycerides, what happens to them

A

combine with bile salt micelles and diffuse to the borders of intestinal epithelial cells

127
Q

T/F bile salts can be recycled after transporting FFA/monoglycerides to the intestinal brush border

A

T; because they are not absorbed until they are in the ileum

128
Q

what happens to a small percentage of bile salts and what is the consequence

A

deconjugated by anaerobic gut bacteria; excreted into feces

129
Q

what is the consequence of bacteria from the colon colonizing the small intestine

A

deconjugation of a large quantity of bile salt -> wash into colon -> diarrhea

130
Q

what happens to conjugated bile salts in the ileum

A

taken up by active Na/bile salt symporter; return to liver via portal vein

131
Q

what 3 disorders would lead to increases in serum bile acids

A
  1. cholestasis
  2. decreased functional hepatic mass
  3. acquired or congenital vascular shunts
132
Q

bile contains other molecules, such as

A

phospholipids, cholesterol, lipid-soluble waste, HCO3

133
Q

how is jaundice an indicator of liver function

A

tells you that fat-soluble waste (i.e. bilirubin in this case) is not being properly eliminated

134
Q

bile release is stimulated in response to what hormones/NTs (2)

A

CCK; ACh from vagus

135
Q

what is digestion

A

breakdown of macromolecules into constituent monomers

136
Q

what is absorption

A

transfer of nutrients from the intestinal lumen to the blood or lymphatics

137
Q

T/F most polymers cannot cross the intestinal epithelium

A

T

138
Q

movement of nutrients, ions and water occurs between what 4 compartments

A

intestinal lumen, cytosol, lateral space, blood/interstitial fluid

139
Q

T/F water and ions can move through tight junctions between enterocytes

A

T (water can also move through aquaporins)

140
Q

water is reabsorbed in normal states because

A

oncotic pressure is greater in capillaries than in the lateral space; it follows reabsorption of nutrients and ions

141
Q

loss of intestinal villi causes diarrhea because

A

reduced area for absorption of nutrients and electrolytes; water stays in intestinal lumen (gets lost osmotically)

142
Q

paracellular transport is (passive/active/both) whereas transcellular transport is (passive/active/both)

A

always passive; active or passive

143
Q

K is absorbed via the ______________ route and occurs primarily in the _____________intestine

A

paracellular; distal (because there is a relatively higher concentration)

144
Q

concentration and electrical gradients for Na are

A

inward

145
Q

Three mechanisms by which sodium absorption occurs are

A
  1. symporters (drives glucose and amino acid absorption)
  2. antiporters (drives H excretion)
  3. simple diffusion (just absorbs Na; negligible)
146
Q

nutrients are absorbed via _______________ route, and rely on __________ transport

A

transcellular; active

147
Q

the 3 types of secretion in the digestive tract are

A

mucus (secreted through multicellular glands in mouth/pharynx/esophagus and unicellular glands in stomach/goblet cells)

specialized substances (such as digestive enzymes) secreted by tubular glands and macroscopic structures (liver, pancreas, salivary gland)

water and electrolytes (crypts of lieberkuhn in intestine)

148
Q

how to crypt cells secrete water and electrolytes (3 steps)

A

1) passive influx of Na/Cl through Cl symporter
2) passive diffusion of Cl out of the cell through Cl channel
3) active pumping of Na out via Na/K pump

water follows the Cl osmotically

149
Q

T/F bicarb is released by salivary glands and the pancreas

A

T

150
Q

what are 3 ways that HCO3 is secreted

A
  1. Na/HCO3 symport (from blood to intestinal cell)
  2. HCO3 channels (limited; tightly regulated; result in H2O secretion and increased pH)
  3. HCO3/Cl antiporter (causes increased pH; important in herbivores)
151
Q

T/F lignin cannot be digested

A

T

152
Q

complex sugars include

A

lactose (glucose + galactose) ; sucrose (glucose + fructose); maltose, isomaltose, maltotriose (di and tri saccharides of glucose)

153
Q

simple sugars include

A

glucose, galactose, fructose

154
Q

simple sugars are absorbed by (2)

A
  1. Na co-transport (symporters; glucose and galactose)
  2. facilitated diffusion (uniporters; fructose)
155
Q

glucose-Na symporter absorbs one glucose/galactose for every ____ sodium

A

2

156
Q

T/F there is a very wide variety of membrane-bound peptidases that break down peptides into free amino acids and di/tri-peptides

A

T

157
Q

once in the cytoplasm, what happens to absorbed di and tri-peptides

A

broken down into amino acids by cytosolic peptidases

158
Q

amino acids are transported into the enterocyte by

A

at least 4 Na co-transporters

159
Q

how are antibodies in colostrum absorbed

A

specialized enterocytes absorb by pinocytosis; reach SI intact because of low HCl and pancreatic enzyme secretion shortly after birth

160
Q

a major form of dietary fats are

A

triglycerides

161
Q

lipid soluble vitamins are

A

A, D, E, K

162
Q

T/F the stomach and tongue produce some lipases that play a role in adult animals

A

F; play a role in suckling animals

163
Q

lipids are absorbed by what mechanisms

A

fatty acid transporter protein; diffusion (when LCFA concentrations in the lumen are high); diffusion for most other lipids

164
Q

once fats are absorbed into enterocytes, what happens

A

triglycerides reassembled and packaged into chylomicrons along with cholesterol

165
Q

chylomicrons are coated with (3)

A

phospholipids, cholesterol and apolipoproteins

166
Q

chylomicrons are absorbed into

A

lacteals -> lymphatics -> systemic circulation

167
Q

electrolytes, minerals and metals are mainly absorbed in the

A

jejunum

168
Q

T/F most ingested calcium is readily absorbed

A

F; most is excreted unabsorbed in feces

169
Q

two mechanisms of calcium absorption are

A
  1. diffusion
  2. vitamin D dependent absorption (opens calcium channels in duodenum; increases expression of calbindin in the cytoplasm)
170
Q

phosphorus is absorbed as

A

phosphate

171
Q

under normal conditions, how is phosphorus absorbed

A

paracellular passive diffusion

172
Q

how does vitamin D regulate phosphorus absorption

A

by insertion phosphorus, Na symporters in the apical membrane

173
Q

how is iron absorbed

A
  1. receptors for protein-bound iron (bound to heme or lactoferrin)
  2. DMT-1 (iron and H+ symporter)
174
Q

what molecule acts as the storage site for iron; how does it store iron

A

ferritin; as ferric iron (Fe3+)

175
Q

what molecule acts as the transporter for iron in the blood

A

transferrin

176
Q

uptake of iron into systemic cells differs from uptake of micelles in enterocytes because

A

the whole transferrin-iron complex is endocytosed; with micelles, the bile salts are not absorbed (only the fats)

177
Q

when iron stores are high, the liver secretes

A

hepcidin (downregulates DMT-1 and transferrin)

178
Q

what is measured to evaluate iron levels

A

plasma transferrin

179
Q

how is copper and zinc absorbed

A

DMT-1 (along with iron)

180
Q

how is Cu and Zn excreted

A

in bile and urine

181
Q

how do you treat Zn sensitivtiy

A

copper supplementation

182
Q

how is vitamin C absorbed

A

Na/vitamin symporter

183
Q

how is vitamin B6 absorbed

A

passive diffusion

184
Q

what needs to happen to vitamin B12 before it can be absorbed

A

needs to first be released from its protein carrier (by HCl and pepsin in the stomach/pancreatic enzymes in the SI)

185
Q

how is vitamin B12 absorbed

A

binds to intrinsic factor in the ileum; complex then binds to receptors on enterocytes and are endocytosed

186
Q

most electrolytes are absorbed best in the

A

ileum and colon

187
Q

during coupled sodium/chloride transport, Na is exchanged for _______________ and chloride is exchanged for _____________

A

H+; HCO3- (Note: both are produced by water and CO2 via CA)

188
Q

how is Cl absorbed in herbivores and why is it important

A

exchange of HCO3 for Cl-; raises the luminal pH which is important to keep a neutral environment when volatile fatty acids are being created by fermentation

189
Q

bicarbonate is mainly reabsorbed in the form of

A

H2O + CO2; driven via Na/H antiporter

190
Q

in horses, what is the junction between the SI and LI; is it normally open or closed

A

ileocecal sphincter; closed (only open during a peristaltic reflex)

191
Q

what are the 3 functions of the cecum and colon

A
  1. absorb water and electrolytes
  2. store feces
  3. ferment and absorb undigested organic material
192
Q

the 3 motility patterns in the cecum and colon are

A

segmentation, propulsion (peristalsis), retropulsion (retroperistalsis)

193
Q

what 2 reflexes promote colonic emptying

A

gastrocolic and duodenocolic

194
Q

colon secretions consist of

A

mucus and HCO3

195
Q

how is mucus/HCO3 secreted in the colon

A

HCO3 channels; HCO3/Cl antiporter

196
Q

T/F VFAs are passively reabsorbed

A

T

197
Q

what vitamins are synthesized by colonic bacteria

A

B, K

198
Q

how are electrolytes and water absorbed in the colon

A

via active absorption

199
Q

diarrhea is

A

increased water content of feces

200
Q

T/F the colon has a large capacity for water absorption, which is increased by aldosterone

A

T

201
Q

the internal colonic sphincter is ___________ under _______________ contrtol

A

smooth muscle; ENS/PSNS (pelvic n)

202
Q

the external colonic sphincter is _____________ under ________________control

A

skeletal; CNS/pudendal n.

203
Q

the defacation reflex is called the

A

rectosphincteric reflex

204
Q

what stimulates colonic peristalsis

A

relaxation of the internal sphincter via PSNS (pelvic n)

205
Q

the three main plant (digestible) wall components are

A

cellulose, hemicellulose, pectin

206
Q

major substrates for fermentation are

A

cell wall components of forages and starches in grains

207
Q

how are carbohydrates fermented in ruminants

A

cellulase (on bacterial surface) breaks down cellulose/hemicellulose/pectin into monosaccharides, which are then absorbed by the bacteria

208
Q

what are the waste products of bacterial carbohydrate fermentation and what is their purpose

A

VFAs; used by ruminant as a source of energy

209
Q

in bacteria, monosaccharides are broken into

A

pyruvate, ATP, CO2 and NADH + H+

210
Q

pyruvate in an aerobic environment yields

A

energy sources (ex. NADH, FADH, ATP and VFAs

211
Q

most bacteria yield what VFA

A

acetate (and methane)

212
Q

lactate is broken down into what

A

acetate and proprionate

213
Q

the main VFAs absorbed by ruminants are

A

butyrate, acetate, proprionate

214
Q

VFA provide what % energy to herbivores

A

60-80%

215
Q

does a high grain or high fiber diet yield more VFA

A

high grain (but VFA in excess will damage the rumen)

216
Q

VFAs are (carbs/lipids/proteins)

A

lipids

217
Q

VFA absorption occurs in what parts of the ruminant stomach

A

rumen, reticulum and omasum

218
Q

as pH drops, rumen papillae _________

A

grow longer (increase SA for VFA absorption)

219
Q

how are VFAs absorbed at a normal rumen pH? what is the net effect

A

bind to H+ (present due to Na/H exchange); HVFA are not ionized and are therefore easily absorbed; acts to increase rumen pH

220
Q

what is the fate of acetate, proprionate and butyrate as an energy source

A

acetate: directly used for energy or to produce lipids
proprionate: converted to glucose in liver and then used for energy
butyrate: converted to β-hydroxybutryic acid in rumen epithelial cells and then used as an energy source

221
Q

β-hydroxybutyric acid is a

A

ketone

222
Q

why can farmers feed ruminants low quality protein

A

bacteria convert any quality protein into high quality protein; when bacteria are digested by the ruminant, it provides high quality protein

223
Q

T/F in ruminants, most amino acids are converted into acetate, proprionate and butyrate

A

T

224
Q

branched-chain amino acids are converted into _______________, which can then be used as _________ for the ruminant or ___________ for the rumen microbes

A

branched chain VFAs, which can be used as an energy source for the ruminant or a growth factor for the rumen microbes

225
Q

protein is ultimately converted to

A

NH3 (ammonia)

226
Q

lipids are digested by microbes into

A

LCFAs

227
Q

T/F ruminants obtain their nutrients by consuming bacteria and their wastes (ex. VFAs)

A

T

228
Q

ruminants can consume bacteria when they

A

are flushed into the abomasum (after proliferating)

229
Q

what can influence the amount of VFAs produced by a ruminant

A

relative abundance of protein and carbohydrate

230
Q

T/F ruminants must synthesize almost all of the glucose that they require

A

T

231
Q

too much grain (rapidly fermentable CHO) can have what consequence; this is called

A

acidify the rumen and alter rumen flora (increased proliferation of lactic-acid producing bacteria, which further decreases pH); grain overload

232
Q

rumen bacteria can synthesize protein from what non-protein nitrogen sources

A

urea, nitrates, ammonia; combined with ketoacids to form amino acids

233
Q

what is a sign that fermentation is complete

A

small dense particles sink from a loss of gas bubbles

234
Q

particles move into the omasum when they are what diameter

A

2-3mm

235
Q

the solid zone contains _______________, the slurry zone contains ______________and the liquid zone contains ___________

A

most recent ingesta (least fermented; moderately fermented ingesta; mostly thoroughly fermented ingesta and water

236
Q

secondary contractions of the rumen cause

A

eructation; removes gas produced by fermentation by bringing it to the region of the esophagus

237
Q

gases at the cardia stimulate

A

gas sensors, that trigger the vagal reflex (by bringing afferent info to the brainstem)

238
Q

what can inhibit eructation and cause bloat

A

froth from young, green forage

239
Q

what stimulates rumination (chewing cud)

A

coarse feed, stretch, and VFA in rumen

240
Q

T/F eructation involves contraction of the reticulum

A

F; regurgitation of cud involves reticulum contraction

241
Q

reticulorumen motility is controlled entirely by

A

vagus

242
Q

how does stretch stimulate rumen motility

A

moderate stimulates; excessive inhibits

243
Q

a large rumen mat _____________ rumen motility
excessively low pH _____________rumen motility
elevated VFA ____________ rumen motility
elevated osmolarity ____________ rumen motility
gases at cardia stimulate __________________

A

stimulates
inhibits
inhibits
inhibits
eructation

244
Q

what happens if cows are fed poor quality feed, especially in cold climates

A

stimulates food intake and movement of ingesta out of the rumen prematurely; gets impaction of abomasum

245
Q

cold climates ______________

A

stimulate rumen motility

246
Q

water half-life in the rumen is

A

15-20h

247
Q

T/F little water moves across the reticulorumen epithelium

A

T

248
Q

when do ruminant rumens become colonized by microbes

A

3-8th week if given access to solid feed

249
Q

in adult cattle, reticular groove closure can occur in response to

A

ADH; water bypasses rumen and is absorbed faster in the SI

250
Q

The abomasum does not ______________, but does secrete ____________, to digest _________

A

absorb nutrients; lysozyme; bacterial cell walls

251
Q

horses have three adaptations to frequent grazing, which are

A
  1. production of large quantities of saliva
  2. loss of mucus production in proximal gastric fundus
  3. continual secretion of gastric acid
252
Q

chewing in horses is important since; as a result, they are given a

A

they cannot regurgitate their feed; high-fiber diet

253
Q

time horses spend chewing creates ___________, which buffer against _____________

A

saliva; gastric acid

254
Q

2 issues with teeth problems in horses are

A

inappetence and decreased volume of saliva (which can lead to gastric ulceration)

255
Q

in horses the proximal fundus is what kind of epithelium

A

stratified squamous

256
Q

what are some problems with intermittent feeding of horses

A
  • do not produce enough saliva to buffer rumen pH -> ulcers
  • VFA production becomes cyclic in cecum/colon -> pH variation
  • feed may be inadequately digested -> colic/diarrhea
257
Q

the equine small intestine is adapted to a low _______, high _______ diet

A

starch; cellulose

258
Q

in the small intestine of horses, digestion and absorption is _________

A

incomplete

259
Q

what is a major difference in digestion in equids vs ruminants

A

in horses, microflora do not enter the intestine, so bacterial CHO, protein and lipid are lost in feces

260
Q

what is a consequence of short transit time in horses

A

loss of protein, carbs and fat in feces

261
Q

pacemakers of cecum/colon transit time in horses are

A

cecum, RVC, pelvic flexure

262
Q

describe the enterosystemic fluid cycle in horses

A

fluid secretion into the intestines equals total extracellular fluid volume; almost all of this is reabsorbed via osmosis as nutrients are absorbed

263
Q

T/F glucose is essentially the only energy source used by the CNS

A

T

264
Q

mobilization of stored CHO begins how many hours after the last meal

A

4-6h

265
Q

glucose ________ diffuses into cells via _______

A

passively; GLUT

266
Q

glut transporters in liver and brain are; in other tissues they are

A

always active; responsive to insulin

267
Q

inside a cell, how is glucose processed

A

glycolysis (to provide energy); glycogenesis; hexose monophosphate; glucuronate

268
Q

in monogastric animals, ____________ fuels the electron transport chain; in ruminants ________________ fuels the electron transport chain

A

NADH; VFAs

269
Q

how to VFAs fuel krebs in ruminants (2)

A

acetate/butyrate become acetyl-CoA
proprionate enters at a diff point

270
Q

what is a major substrate for gluconeogenesis in ruminants and where is it diverted from

A

oxaloacetate; Krebs cycle

271
Q

in the liver, phosphorylation of glucose is _________ by insulin and ____________ by lack of insulin

A

increased; decreased

272
Q

the hexose monophosphate pathway is involved in production of __________________, reduction of ____________, and synthesis of _____________

A

fatty acids and steroids; glutathione; nucleic acids

273
Q

the glucuronate pathway is involved in synthesis of ________________, _________________ and is required for some forms of _____________ metabolism

A

proteoglycans, vitamin C, hepatic

274
Q

When pyruvate accumulates during exercise, it is converted into lactate and travels to the liver. In the liver, it is used to resynthesize glucose. This process is called

A

the Cori cycle

275
Q

1) HDLs add __________ apoproteins to the chylomicron, making it a ______

2) ApoC activates what on the capillary endothelium

3) lipoprotein lipase does what

4) the chylomicron then loses _____, which signals for it to be absorbed by the __________ and recycled into _________; it may also be taken up by other cells that require ____________

A

apoC and apoE; VLDL

lipoprotein lipase

hydrolyzes TGs into LCFAs and monoglycerides

Apo C; liver; new VLDLs; new cholesterol

276
Q

in adipose, LCFAs are ________; in other tissues they are _________

A

resynthesized into TGs; oxidized for energy

277
Q

in order to be destroyed, chylomicron remnants must have

A

ApoE

278
Q

HDLs are synthesized in (2)

A

liver and small intestine

279
Q

The 2 functions of HDLs are to

A

retrieve ApoC and transfer ApoC/ApoE to new chylomicrons; transport cholesterol to the liver

280
Q

the liver can do what to HDLs

A

endocytose them and incorporate their components to form new VLDLs

281
Q

LCFAs created via the endogenous pathway are transferred through the blood on ___________________; triglycerides synthesized by the liver are transported through the blood stream by _____________

A

albumin; VLDLs

282
Q

if the cell has sufficient energy, non-ruminants can divert what from the Krebs cycle for synthesis of LCFAs; this occurs in the ________

A

citrate; liver

283
Q

in ruminants, what can be used to create LCFAs; this occurs in the ______________ and _______________

A

acetate; adipose and mammary tissue

284
Q

in regards to mobilization of stored TG, insulin _______ and glucagon _________; thyroid hormone _____________ utilization of circulating lipids

A

inhibits; promotes; promotes

285
Q

inherited defects in lipoprotein lipase can cause

A

hyperlipidemia

286
Q

what are ketones

A

normal, water-soluble metabolites of lipids

287
Q

ketones can be used in what context

A

in place of glucose to provide acetyl-CoA for Krebs

288
Q

T/F acetone contributes to keto-acidosis

A

F; it is a weak acid, and is relatively volatile, so it is exhaled

289
Q

T/F acetoacetate and B-hydroxybutyric acid are ketones that act as strong acids at normal blood pH

A

T

290
Q

under normal conditions, ketones are used for _______ in ________ tissues

A

ATP production (converted back into acetyl-CoA); non-hepatic

291
Q

T/F the liver is able to utilize ketones for energy

A

F

292
Q

what is the main ketone in ruminants that contributes to ketacidosis

A

β-hydroxybutyric acid

293
Q

For what 2 reasons are ruminants prone to keto-acidosis

A
  1. they have 2 sources (LCFAs from adipose and VFAs from fermentation)
  2. they must synthesize all of their glucose by diverting oxaloacetate, which causes more ketone formation when fat is mobilized
294
Q

what are the main causes of keto-acidosis

A

Anything that mobilizes large amounts of fat
- starvation or anorexia
- lactation or late pregnancy
- insulin deficiency

295
Q

T/F the most over-conditioned animals are least likely to develop keto-acidosis

A

F; they are the most likely

296
Q

why does fat mobilization predispose animals to fatty liver? how does this coincide with gluconeogenesis in a state of anorexia

A

if TG formation exceed the hepatocytes ability to form VLDLs, lipid droplets form -> can destroy hepatocytes; in a state of anorexia, you also get diversion of oxaloacetate, which means the mitochondria take up less LCFA, and more is converted to TG in the cytoplasm

297
Q

why are cows prone to fatty liver?

A

less efficient at exporting VLDLs AND they divert more oxaloacetate under normal conditions

298
Q

give 3 reasons why pregnant or lactating ruminants are especially prone to fatty liver and ketosis

A
  1. less efficient at transporting VLDLs (buildup of TG more likely)
  2. divert more oxaloacetate (more formation of ketones; less use of LCFAs that can be converted to TGs)
  3. more prone to insulin resistance (more mobilization of LCFAs)
299
Q

why might ketones appear in the urine

A

during ketosis, the absorption capacity of renal tubular epithelium is saturated

300
Q
A

Veterinary Physiology (11 decks)

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