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MONOGASTRIC GI > 2 – Functional Development of the GIT > Flashcards

2 – Functional Development of the GIT Flashcards

1
Q

Mammals at birth:

A

-an immediate change from amniotic fluid to milk

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2
Q

Mammals at weaning:

A

-gradually (or immediate) change from milk to solid food

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3
Q

Weight of fetus in utero:

A

-increases dramatically during the last 1/3 of gestation
*associated with marked growth in GIT

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4
Q

Adrenal gland develops:

A

-rapidly during later 1/3 of gestation
*cortisol is thought to be an important mediator of GIT development in utero

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5
Q

Development of gastric function in utero:

A

-increases in stomach acid and gastrin secretion
-some other enzyme activities (chymosin, pepsin, amylase, lactase, aminopeptidases)

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6
Q

Stomach development:

A

-thickening of glandular region
-maturation of chief cells (secrete zymogens, inactive enzymes)

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7
Q

Stomach development following birth:

A

-volume of pepsin and HCl increase gradually
>species specific
-pH is higher
-HCl secretion begins 1-2 days post birth

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8
Q

Small intestine development:

A

-increases in length and diameter from birth to adulthood
-crypts and villi organized and functioning at birth
-enzymes present at birth

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9
Q

Enzymes present in small intestine at birth:

A

-lactase levels are higher in neonate than adult
-alkaline phosphatase activity is minimal at birth, increases gradually

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10
Q

Early postnatal the SI is permeable to:

A

-large molecules

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11
Q

Allometric growth:

A

-not everything grows linear
*organ specific
Ex. body doubles in size, does not mean small intestine doubles in size

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12
Q

Post natal increase in small intestinal weight:

A

-gains weight faster than other tissues when suckling
-loss weight faster when food-deprived

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13
Q

Work dogs and small intestine during postnatal development:

A

-decrease in length, weight, and SA from weaning to adult
-decline in villus height
-increase in crypt depth following weaning

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14
Q

What is important when using milk replacer?

A

-want milk from the same species

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15
Q

Does creep feed help with the weaning transition:

A

-decreased vilus height/crypt depth due to weaning regardless of given creep or not
>varies along the small intestine
*effect of weaning is seen along entire small intestine
*gradually weaning can help a lot

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16
Q

Weaning in dogs and small intestine:

A

-decrease in lactase activity proximal to distal
>decrease with age
-peptidases: less of an effect due to intestinal segment
>tendency of dipeptidase IV to increase with age

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17
Q

Effect of age and weaning in pigs on activity of pancreatic enzymes:

A

-amylase increases in response to animal receiving solid feed
>decreases and then increases again

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18
Q

Summary of GIT at birth and weaning:

A

-adapted at birth to digest milk components
-development of digestive enzymes is AGE and DIET dependant
*weaning is an insult to GIT and results in temporary reduction in enzymatic activity

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19
Q

Barrier function:

A

-controls entry into animal of substances that may be toxic/infectious if they freely enter
-forms a barrier to ‘outside’
*achieved by epithelial cells joined together by tight junctions

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20
Q

Intestinal barrier consists of:

A

-apical and basolateral barrier
-nutrients travel by paracellular transport
*ABC transporters – ATP binding cassette

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21
Q

Dysfunction of intestinal epithelial barrier results in:

A

-‘leaky gut’
>associated with intestinal disorders

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22
Q

Leaky gut and intestinal disorders examples:

A

-IBD
-Crohn’s disease
-ulcerative colitis
-diabetes
-COPD

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23
Q

What are the main components of the GI barrier?

A

-epithelial barrier
-mucus barrier
-lamina propria (subepithelial region)

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24
Q

Epithelial monolayer is composed of:

A

-absorptive enterocytes (single layer)
-goblet cells (mucous)
-intestinal epithelial cells (IECs)
-Paneth cells
-enterochromaffin cells
-stem cells

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25
Q

IECs:

A

-phagocytose bacteria
-neutralize toxins

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26
Q

Paneth cells:

A

-secret anti-microbial peptides

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27
Q

Enterochromaffin cells:

A

-neuroendocrine cells

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28
Q

Mucous barrier is above epithelial barrier and is composed of:

A

-mucin
-secretory
-sIgA dimers
-antimicrobial peptides
*first barrier to pathogens

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29
Q

What are the chemical and physical mechanisms of the barrier function?

A

-microbiota
-chemical
-physical
-immune

30
Q

Chemical mechanism of the barrier function:

A

*first line of defense
-microorganisms
-IgA
-mucins
-antibacterial peptides

31
Q

Physical mechanism of the barrier function:

A

-intestinal epithelial cells
-goblet cells
-Paneth cells
-intestinal stem cells

32
Q

Layers of the intestinal epithelial gut barrier:

A

-microflora
-mucus
-intestinal epithelium
-lamina propria

33
Q

Microflora:

A

-competes with pathogens for nutrients
-metabolizes proteins and CHO
-synthesizes vitamins
-produce metabolic products that ‘communicate’ with gut, brain and immune system

34
Q

Mucus:

A

-varies throughout intestine
-small intestine: thin layer facilitating absorption
>glycoproteins, secretory IgA, antimicrobial peptides

35
Q

Intestinal epithelium:

A

-tight junctions
-monolayer of cells
-immune functions

36
Q

Lamina propria;

A

-innate and adaptive immune cells

37
Q

Why is low protease activity at birth adaptive?

A

-allows for acquisition of passive immunity
>don’t want to digest other enzymes or immune proteins

38
Q

What is a critical function of the intestinal epithelial cells (IECs)?

A

-to maintain barrier integrity via tight junctions
-TOP to BOTTOM:
>adherens junctions
>desmosomes
>gap junctions

39
Q

Adherens junctions:

A

-important for cell signaling
-stabilization of cell-to-cell adhesion
-participate in cell proliferation
-establish polarity
-remodelling of actin-cytoskeleton

40
Q

How do adherens junctions regulate adhesion?

A

-through transmembrane adhesion molecules associated with actin

41
Q

Desmosomes:

A

-‘leaky’
-mechanical strength
-intercellular junctions
-important for intercellular signalling

42
Q

Gap junctions:

A

-allow transport of small molecules
>communication between cells
-regulatory role in cell growth and differentiation
-6 transmembrane proteins

43
Q

Tight junctions:

A

-formed by proteins
-permeability seal
-facilitate communication between cells
-selectively limit diffusion of molecules, water and ions
-protect against inflammation and infection

44
Q

How are tight junctions regulated?

A

-arrangement of actin with interaction of transmembrane proteins to form a tight seal
>occludins
>claudins
>junctional adhesion molecules (JAMs)

45
Q

How is the complex in tight junctions strengthened?

A

-zona occluden proteins (ZO-1, ZO-2, ZO-3)
>bind to actin filaments

46
Q

Tight junctions are highly regulated by:

A

-phosphorylation of occluding proteins to open and close

47
Q

What happens to tight junctions when stressed?

A

-damaged due to response of stressor
>*leaky gut

48
Q

Leaky gut leads to:

A

-LPS, pathogens and non-digested food particles allowed to enter bloodstream
>immune system activation and inflammation
>infections, antibiotics, dysbiosis

49
Q

Probiotics:

A

-show to be effective for maintenance of intestinal integrity
-anti-inflammatory

50
Q

Dietary fiber and short chain fatty acids (SCFA):

A

-deficiency in SCFAs impairs barrier function

51
Q

What are some factors that can affect intestinal barrier integrity?

A

-high fat diet
-drugs/antibiotics
-genetic susceptibility
-pathogens
-environmental stress
*weaning
*all lead to altered microbiota and damage to epithelial layer

52
Q

What gut diseases can you get from a damaged epithelial layer?

A

What gut diseases can you get from a damaged epithelial layer?
-inflammatory
-metabolic
-systemic

53
Q

Inflammatory diseases:

A

-ulcerative colitis
-Crohn’s disease
-Coeliac disease

54
Q

Metabolic diseases:

A

*metabolic endotoxemia=low grade systemic inflammation
-obesity
-diabetes

55
Q

Which diets are associated with an increased risk of leaky gut?

A

-high in:
>sucrose
>refined CHO
>PUFA (omega-6)
-low in fiber

56
Q

What are the 3 layers of FETAL membranes?

A

-endothelium
-connective tissue (chorioallantoic mesoderm)
-chorionic epithelium (outermost layer)

57
Q

What are the 3 potential layers of maternal membranes?

A

-endothelium
-maternal connective tissues
-maternal endothelial cells

58
Q

Epitheliochorial placenta type:

A

-all 3 maternal layers retained
Ex. horse, swine, ruminants

59
Q

Endotheliochorial placenta type:

A

-only uterine endothelium retained
Ex. dogs, cats

60
Q

Hemochorial placenta type:

A

-no maternal layers retained
Ex. humans, rodents

61
Q

Incomplete barrier function in immature gut is important for:

A

-species with placenta that restricts macromolecular transfer in utero
*allows transfer of large molecules (ex. immunoglobulins)

62
Q

Immature enterocytes (fetal) possess:

A

-high endocytic capacity for macromolecular passage
-ceases at ‘gut closure’ (barrier function is now intact)
>timing varies among species

63
Q

Ungulates:

A

-placenta is effective barrier
-born agammaglobulinemic
-extensive macromolecular transmission during first days of life
-endocytosis, non-selective

64
Q

When does ungulate duodenum, jejunum closure occur?

A

-1-2 days

65
Q

When does ungulate distal small intestine closure occur?

A

-2-3 weeks

66
Q

Carnivores:

A

-some maternal IgG transmitted over placenta
-main macromolecular transfer from colostrum
*gut closure in 1-2 days

67
Q

Primates:

A

-extensive, selective transfer across placenta
-receptor mediated binding of IgG to FcRn receptors
>especially during late gestation
-humans gut closure is ~22weeks

68
Q

Rodents:

A

-species dependent
-post-natal expression of FcRn receptors that bind IgG as well as other milk proteins
>more specific transfer
*gut closure is later (~3 weeks)

69
Q

Guinea pigs:

A

-receive IgG in utero

70
Q

Rats and mice:

A

-limited transfer in utero
-postnatal transfer is important

71
Q

Timing of intestinal barrier closure in puppies and administration of colostrum:

A

-8hrs: 50% IgG absorption
-12-16hrs: slightly increase but not maintained
-24hrs post birth: no IgG absorption

MONOGASTRIC GI (24 decks)

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