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digestion and metabolism - Wk 3 > large intestine physiology > Flashcards

large intestine physiology Flashcards

1
Q

what are tenia coli

A

three longitudinal smooth muscle bands around the large intestine

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2
Q

what are haustra

A

small pouches generated by sacculation, due mainly to tenia coli shorter length

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3
Q

what is SCFA production - fermentative digestion

A

non-enzymatic digestion by microbes which produce short-chain (volatile) fatty acids (SCFA or VFA). similar to bovine rumen

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4
Q

what are the 3 VFA

A

acetate, propionate, butyrate

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5
Q

what do VFA do

A

ferment hydrolysable nutrients that escape digestion/absorption in SI and indigestible complex molecules that reach LI intact

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6
Q

how much energy do horses obtain from SCFA produced in the ceum

cencum and ventral colon

A

30%

up to 70% horses energy from LI

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7
Q

what is butyrate

A
  • respiratory fuel for colonic epithelium
  • downregulates inflammatory genes
  • maintains epithelial homeostasis
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8
Q

what is propionate

A

used by liver as precursor for gluconeogenesis

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9
Q

what is acetate

A

used by peripheral tissues and precursor for lipogenesis

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10
Q

small amounts of lactic acid is…

A

poorly absorbed and not a major nutrient

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11
Q

increased amounts of lactic acid…

A

intraluminal acidosis and increase in intraluminal osmolality - disease

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12
Q

proteins produced by microorganisms are …

A

not usable b/c amino acids and proteins are not absorbed from large intestine

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13
Q

nitrogen excretion

A
  • synthesis of microbial protein consumes non-protein nitrogen
  • traps nitrogen in the lumen of the LI
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14
Q

what makes up the microbiome

A

bacteria, protozoa, fungi, archaea, viruses, parasites

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15
Q

high diversity and species richness is associated with

A

health

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16
Q

LI is a relatively ____ environment compared to the upper GI tract

A

stable

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17
Q

what does a hay diet produce

A

a more stable microbiome

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18
Q

clostridia

A

major SCFA producer

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19
Q

lachnospiraceae and ruminococcaecae

A
  • butyrate - critical for mucosal health and depleted in disease
  • turns lactate into acetate and propionate
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20
Q

streptococcus

A

amylolytic, lactate producer

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21
Q

lactobacillus

A

lactate producer

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22
Q

what does the ratio of VFA:lactic acid depend on

A

diet
* grain = more propionic and lactic acid - decreases intraluminal pH
* grain decreases ruminococcus and fibrobacter, clostrodoales, lachnospiraceae

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23
Q

what is toxic to LI microbiota

A

fat
* high oil, increases proteobacteria

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24
Q

what happens when there is a decrease (<50%) firmicutes

A

disease (colic)

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25
Q

what happens when there is an overabundance in proteobacteria (upper GI)

A

diease (colic)

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26
Q

what are the functions of the LI

A
  • supply nutrients, water, electrolytes, VFAs, and vitamins
  • maintain ideal environment for microbiome
  • protect mucosa
  • maintainlow viscosity of digesta and lubricate mucosa
  • excrete substances such as nitrogen and potassium
  • occurs via crypts and surface epithelium
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27
Q

what is the LI a reservoir of

A

water and electrolytes

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28
Q

what percent of a horses body weight do they secrete water and electrolytes into their digestive tract daily

A

30%

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29
Q

what are the primary electrolytes that are secreted

A

Cl-, Na+, HCO3-, PO43-

affected in diarrhea

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30
Q

water secretion is ____ driven by osmotic gradient generated by solute secretion

A

passive

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31
Q

what is electrolyte secretion driven by

A

electrocgenic Cl- secretion

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32
Q

how is Na+ and K+ secreted into lumen

A

paracellular pathways

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33
Q

what are the electrolytes that are primarily absorbed

A

Na+,K+, Cl-, P

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34
Q

how is Na+ actively absorbed

A

by electrochemical gradient generated by Na+/K+ ATPase

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35
Q

what is electroneutral Na+ absorption

A
  • Na+ exchanged for another cation (H+)
  • coupled with Cl- and VFA absorption in exchange for HCO3-
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36
Q

what is electrogenic Na+ absorption

A
  • sodium absorbed against electrochemical gradient
  • uncoupled entry of Na through Na channels - epithelial sodium channel
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37
Q

what is electrogenic Na+ absorption regulated and inhibited by

A

aldosterone and diuretics that close the sodium channels

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38
Q

how is K+ acitvely absorbed

A

in exhange for H+ via H+, K+ ATPase

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39
Q

how is Cl- passively absorbed

A

with cations (Na+) via paracellular pathways and by Cl- HCO3- echange through transcellular pathway

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40
Q

how is P diffused

A

paracellular pathways

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41
Q

____ movement of water occurs ____ along hydrostatic, oncotic, and osmotic gradients

A

bidirectional; passively

42
Q

hydrostatic gradient

A

interstitial - capillary pressure

43
Q

oncotic gradient

A

interstitial - capillary pressure (macromolecule conc.)

44
Q

osmotic gradients

A

intestinal lumen, cytoplasm, interstitial space, capillaries
* electrolytes (Na+), VFAs
* affected by absorption, secretion, and intraluminal fermentation

45
Q

what is the main mechanism of absorption of SCFA

A

transcellular diffusion of protonated SCFAs

46
Q

what is required in the absorption of SCFA

A

high H+

47
Q

SCFA are absorbed in echange for

A

HCO3-

48
Q

what are vesicles and what are they dependent on

A
  • monocarboxylate transporter protein
  • pH, time, concentrate
49
Q

what is the order of VFA/SCFA of absorption

A

acetate>propionate>butyrate

50
Q

what is indirect regulation of LI secretion and absorption

A

motility, capillary hydrostatic pressure

51
Q

what is direct regulation of LI secretion and absorption

A

direct control of epithelial ceells - autocrine, paracrine, endocrine, immunologic, neurocrine mechanisms

52
Q

what do regulatory cells function as

A

sensors or connected to other cells with capacity to respond to stimuli (low systemic blood pressue, hyperkalemia)

53
Q

what is sympathetic stimuli of LI regulation

A

pro-absorptive

54
Q

what is parasympathetic stimuli of LI regulation

A

anti-absorptive/pro-secretory

55
Q

what are Na and water regulatory mechanisms

A
  • renin-angiotensin-aldosterone - decreases secretion/increases absorption NaCl and water
  • catecholamines & aldosterone - increases water absorption
  • angiotensin II - increases electroneutral Na+ absorption
  • aldosterone - increases electrogenic Na+ absorption via increase expression of Na+ channels and N/K pump and increases electroneutral Na+ absorption
  • vasopressin - increases water absorption
  • atrial natriuretic peptide released by heart in response to atrial wall stretching secondary to hypervolemia - decreases Na+ and water absorption
56
Q

what are the interstitial cells of Cajal

A
  • electrical pacemaker cells of GI tract in submucosa - spontaneous electrical and mechanical activity of smooth muscle
  • bipolar cells or spindle shaped
  • don’t form their own network
  • generate slow waves - smooth muscle cells - depolarizaiton - Ca ion entry - phastic contractions - peristalsis and segmentation contractions
57
Q

what are the functions of motility

A
  • mixing digesta
  • contact intestinal contents w/ mucosa
  • adequate time for fermention and absorption
  • transit for defecation and empyting colon
  • transit slower than SI
58
Q

digesta moves from ileum through the ____ into the cecum

A

ileocecal valve (one-way valve)

59
Q

horses eating roughage contents from ileum to ____

A

cecum is 90% water

60
Q

what is partially filled with watery digesta

A

cecum

61
Q

what is the cecal base filled with

A

has at pressure slightly negative to relative atomospheric

62
Q

cecal contents empty into right ventral colon through

A

cecocolic orifice

63
Q

how is digesta moved through the cecocolic orifice

A
  • muscular contractions form a contriction at cecal base cranial to ileocecal papilla - cranial and caudal compartments & elevation of ventral cecal base and opening for cecocolic orifice
  • contraction of cranial comp. of cecal base moves digesta and gas from cecum - right ventral colon
  • large amounts of digesta move bacl to cecal body (from base)
64
Q

what prevents reflux of digesta

A

sigmoid configuration of cecolic juction

65
Q

where are fecal balls formed

A

decending colon
* secretion increases mucus and this decreases resistance to passage

66
Q

what are the functions of mucus produced by goblet cells

A
  • physical barrier against acids, microbial products, food particles, food-associated toxins, first-line defense against microorganims
  • lubricates luminal contents; facilitates digesta transit by minimizing friction with mucosa (descending colon)
  • maintains intestinal homeostasis; immunology
67
Q

what is the structure of mucus in the LI

A
  • branched glycoproteins; interact with external environment via hydrophilic nature influence viscosity
  • two mucus layer in colon: inner and outer
68
Q

what is the structure of the inner layer of mucus

A
  • secreted by surface goblet cells
  • anchored to surface goblet cells/adhered to mucosal epithelium
  • stratified and organized as a filter to separate epithelium from microorganisms - no bacteria
  • endogenous protease activity and slow expansion to 2-3x volume increases the pore size and allows bacteria to penetrate forming outer later
69
Q

what happens if there is no mucus

A

bacteria come in contact with epitheloum and cause inflammation and can lead to cancer

70
Q

what is the structure of the outer layer of mucus

A
  • loosely adhered
  • harbors bacteria
  • bacterial flora and cytokines regulate penetrability
  • energy source for bacteria
  • mucus viscosity increases toward the distal GI tract and determines the spatial distribution of the microbiome
71
Q

what is regulated vesicle secretion

A
  • fusion of single mucus vesicle membrane with plasma membrane
  • regulated by typical vesicle exocytosis components
72
Q

what is compound exocytosis

A
  • all mucus granules fused together and empty the mucus as a single layer
  • more dramtic and whole cell explodes
  • critical in maintaining intestinal barrier
73
Q

what do surface goblet cells have

A

rapid mucin synthesis and secretion with little storage

74
Q

what are upper crypt goblet cells

A
  • slower secretion
  • mucus accumulates in granules
75
Q

how is mucus production regulated

A
  • endocytosis, autophagy, ROS generation, inflammasome assemly and activation
  • regulated by intracellular Ca2+ and Ca2+ mobilizing agents (ACh and histamine)
76
Q

what mobilizing agent does the colon only respond to

A

histamine

77
Q

what does ACh target

A

crypt goblet cells by activating M3 muscarinic receptors leading to mobilization of Ca2+

78
Q

what is the rectum

A

temporary storage of feces before defecation

79
Q

what are the two main anal sphincters

A
  • internal anal sphincter: controlled by parasympathetic fibers; involuntary
  • external anal sphincter: skeletal muscle controlled by somatic nerve supply from inferior anal branch of pudendal nerve; voluntary
80
Q

what does defecation involve

A

integrationof peristalsis on most colonic regions (gastrocolic reflex)

81
Q

pre-defecation

A

increased propulsive peristaltic waves

82
Q

sensation of defectory urge

A

increased propagative peristalsis

83
Q

how does defecation occur

A
  • feces contact receptors in upper anal canal - relax inner anal sphincter - defecatory urge
  • rectal walls expand with feces - stretch receptor stimulation - defecatory urge
  • defecatory urge - initial voluntary contraction of the external anal sphincter
84
Q

what does rectal evacuation require

A
  • correcting angle rectum
  • contraction of abdominal muscles and diaphragm
  • relaxation of pelvic wall muscles
  • relaxation of external sphincter
  • peristalsis then facilitate the movement of feces through the anal canal
85
Q

what are the epidemiologies of management factos that affect LI function

horses

A
  • increase hours in stall/decrease exposure to pasture
  • recent travel within 24 hrs
  • crib-biting/windsucking
  • recent change in diet
  • poor hay quality
  • high concentrate diet
  • recent change in exercise
  • inadequate parasite management
  • inadequate dental care
86
Q

what does poor feed quality cause

A

impaction at pelvic flexure in left ventral colon

87
Q

when do most impactions occur

A

in winter b/c decreased water intake and change in diet

88
Q

what does meal feeding cause

A

increase in volumes of water secreted into the GI tract - hypovolemia - renin-angiotensisn-aldosterone - increase Na+ absorption - impaction

89
Q

what do high concentrate meal feeding cause

A
  • increase secretion of large fluid vol. into SI - transient hypovolemia - increase renin-angiotensin-aldosterone - increase colonic fluid absorption
  • decrease SI transit time - increases fermentable soluble CHO in cecum/colon - increases renin-angiotensin-aldosterone - increases colonic fluid absorption
  • dysbiosis
90
Q

what happens in horses moving from pasture to a stall with contolled exercise

A
  • decrease fecal output
  • increase fecal dry matter content
  • increase water consumption
  • decrease colonic motility
91
Q

what are laxatives

A

substances that promotes bowel movements

92
Q

what is an example of a bulk-formin laxative

A

psyllium

93
Q

what is an example of a lubricant laxative

A

mineral oil

94
Q

what is an example of a hypersmotic and saline laxative

A

MgSO4

95
Q

what is the main laxative that is mostly used

A

water and electrolytes

96
Q

what is salmonella sp.

A
  • faculative anaerobe
  • intracellular pathogen
  • ingested from fecal contaminated feed
  • entrapped in esophageal mucus
  • survive gastric acidity
  • colonizes digestive tract
97
Q

what do dead salmonella produce

A

endotoxin (LPS) causing colitis

98
Q

where does salmonella invade and multiply

A

enterocytes

99
Q

how does salmonella attach to enterocytes

A

fibrial appendages

100
Q

what are clinical features of salmonella

A
  • colic
  • diarrhea
  • systemic inflammatory response
  • hypovolemic shock
  • electrolyte disturbances
  • hypoproteinemia/hypoalbuminemia
  • pre-renal/renal (AKI) failure
  • laminitis
101
Q

treatments of salmonella

A
  • IV fluid & electrolyte therapy
  • colloidal support
  • analgesia
  • digital cryotherapy
  • +/- antimicrobials
  • antidiarrheal (absorbs bacterial toxins - biosponge)

digestion and metabolism - Wk 3 (5 decks)

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