Ruminant GIT Flashcards

Covers cards for all of the rumen and a little bit on the monogastric stomach

1
Q

What are ruminal papillae affected by?

A

The concentration of VFAs

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2
Q

How will high VFA diets affect the papillae of a ruminant?

A

High VFA= long luxuriant VFA

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3
Q

What volatile fatty acids are produces in the ruminant?

A

Acetic acid
Butyric acid
Propionic acid

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4
Q

What is the precurser of propionic acid?

A

Propionate

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5
Q

What is the major product of nutrient digestion?

A

pyruvate
pyruvate is converted to VFAs for microbiota

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6
Q

Describe the absorption in the forestomach

A

Water flows in and out based on osmolarity
AT of Na maintains electro gradient
VFA absorbed and transported to liver
Ions reabsorbed and recycled

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7
Q

Where are VFAs absorbed?

A

Through rumen wall and some through omasum

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8
Q

Why is cellulose difficult to digest?

A

Low surface area to vol ratio
Ruminants do not have enzymes to break down cellulose

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9
Q

How can ruminats break down cellulose?

A

Cudding -Chewing food and regurgitating and reswallowing
Musc contraction of the rumen affects SA:V ratio and inc microbial fermentation

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10
Q

What is the reticuloomasal orifice?

A

Sphincteral structure which forms the connection between the reticulum and the omasum
Ingest must pass through before reaching distal digestive tract

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11
Q

How can ruminants get the enzymes to break down cellulose?

A

Microbiome bacteria have the correct enzymes
Bacteria digest cellulose and release VFAs

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12
Q

What are the functions of the rumen microbiome?

A

Bacteria w diff enzymes
Bacteria act on diff substrates so produce different products = food web

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13
Q

What is the diet of the rumen microbiome?

A

Cellulose
Lignin
Starch
Oil
Protein

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14
Q

Why is the rumen microbiome a symbiotic relationship?

A

Bacteria = protection and nutrients
Rumen = VFAs in return

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15
Q

How is an anaerobic environment maintained in the rumen?

A

O2 entering is soaked up by bacteria to maintain conditions
Involves methanogens in terminal stages of degradation organic material in An conditions

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16
Q

What is the function of microbial fermentation?

A

High quality feed from poor
adds nitrogen from non protein nitrogen sources
Incorporates carbon into microbial proteins and nucleic acids
Provides essential AA

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17
Q

How is fibre digested in the rumen?

A

Broken down by protozoa in the microbiome

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18
Q

How do anaerobic fungi help break down fibre?

A

Enzymatic breakdown using hemicellulose, cellulases, xylanases, glycosidases
Increase surface area

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19
Q

What are archaea?

A

A group of microorganisms similar to but evolutionarily distinct from bacteria
Extremophiles

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20
Q

Role of Archaea in rumen?

A

Range of diff metabolisms including methanogenesis
This uses H and Co2
Good bc H needs to be removed from rumen for conditions

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21
Q

What is involved in the rumen examination?

A

Position examination
Abdominal silhouette
Faecal examination
Rumen fill scores

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22
Q

What is the reticulum?

A

Crescent shaped struct w smooth contour that collects smaller digesta and moves them to the omasum while larger particles remain in the rumen

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23
Q

What is the internal structure of the reticulum?

A

Tissues in the reticulum form a network similar to a honeycomb

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24
Q

Where is the reticulum in relation to the rumen?

A

Adjacent to the diaphragm, lungs abomasum, rumen and the liver

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25
Q

What is the ruminoreticulum?

A

Small tissue fold between the reticulum and the rumen (the two arent separate compartements)

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26
Q

How do ruminants regurgitate ingesta?

A

initiated w a reticular contraction distinct from primary contraction
Contraction in conjunction with the relaxation of the distal oesophageal sphincter allows a bolus to enter oes

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27
Q

What are the two kinds of ruminal contractions

A

Primary - mixing
Secondary - eructation

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28
Q

Describe primary ruminal contractions

A

Originate in the reticulum and pass caudally around rumen
Wave contraction followed by a wave relaxation

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29
Q

Describe secondary contractions

A

Only occurs in some parts of the rumen

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30
Q

What is the 3rd contraction of the rumen?

A

Facilitates remastication

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31
Q

Describe the primary rumen motility pattern

A

Initiation of cycle by a double reticular contraction
1st ret contraction
2nd- ret contraction evacuates particles through ROO
Cont of cranial retrum fold moves material in dorsal sac followed by vent sac
Ventral sac cont moves dense material to the reticulum

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32
Q

Describe the second rumen motility pattern

A

Dorsal sac contr cranially to caudally moving gas cap forward
ret and Reticuloruminat fold reflex
Exposed cardia opens and gas enters oes
Ventral sac contracts caudal to cranial and retrum fold relaxes
Dense material moves forward into the sac

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33
Q

Describe the nervous control over ruminal motility

A

Rich ENS system
Coordinated contractions from cns in brainstem via vagal efferent nerve

Vagal efferent nerves from rumen to motility centres allows stretch receptors and chemoreceptors to modulate contractility

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34
Q

Rumen contraction timings

A

3 rumen contractions every 2 mins

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35
Q

How does ruminal motility affect the food?

A

Food sits in layers
rumen shakes form side to side so separates food into density layers

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36
Q

What is the importance of forestomach motility?

A

Continous mixing of bacteria and food
Retains ingesta for microbial digestion and down sizing of particles
Appropriate env by removing gas

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37
Q

Describe the location of the abomasum

A

Located in the ventral abdomen to the right of the midline in the cranial abdomen in the sheep

38
Q

What is a displaced abomasum?

A

movement of abo out of normal position
L: Caught between rumen and left abd wall
R: Abomasum moves up right wall and is trapped above the omasum

39
Q

What are the effects of an LDA?

A

Stretching = constriction of exit from abomasum = gas therefore a ping is heard at rib 9-13 on left

40
Q

What is the effect of an RDA?

A

Constricts outflow from the abomasum= gas
Twists all the way over = colic

41
Q

How does the omasum and abomasum work together?

A

Omasum = pump the aspirates ingesta and transfers to the abomasum

42
Q

What is the structure of the abomasum?

A

Fundus, body pylorus
Longitudinal rugae
Columnar epithelium
glands
no pyloric sphincter - wall thickening instead

43
Q

What is the normal pH of the abomasum?

A

3.4

44
Q

What are the stomachs of the ruminant and their functions?

A

Rumen - fermentation vat
Reticulum - part of the rumen
Omasum - Water absorption
Abomasum- true stomach

45
Q

Describe the anatomical location of the rumen

A

Located on the left - moves all viscera to the right
Liver is at 6-12 o clock rotation

46
Q

What lines the rumen?

A

keratinised epithelium ( has own blood supply so is able to absorb nutrients and water)

47
Q

What is the structure of the ruminal papillae?

A

Leaf shaped
Keratinised
Poorly developed in the roof of the dorsal sac
Absorb VFAs

48
Q

What lines the reticulum?

A

Series of keratinised cells with smaller cells inside
Have conical papillae

49
Q

How will feed quality affect the time spent in the rumen?

A

Poorer = longer in rumen
Rough hay = more time in rumen
Ruminants are supposed to be slow digesters

50
Q

Describe the structure of the omasum?

A

Broadly spherical with flattened sides
COntains lost os laminae which are covered with conical papillae
Laminae in 3 size groups

51
Q

Describe the motility of the omasum

A

regular biphasic contractions squuze materials into the rececesses
General contraction pushes fluid forward

52
Q

What are the major omasal anatomical structures?

A

Omasal canal
Reticuloomasal orific
Omasal abomasal orifice
Omasal leaves

53
Q

How is milk digested in the ruminant neonate?

A

Digested in the abomasum
Fundus glands = rennin = coagulates casein in acid env
Clot retains milk to allow complete digestion by pepsin

54
Q

What is the reticular groove in the ruminant?

A

In neonates
Acts as a diversion for milk

55
Q

What is the reticular groove reflex?

A

Stim by vagus nerve - ~Groove contracts to create a tunnel between the oes and the reticuloomasal orifice

56
Q

How does the size of the chambers change as the neonate grows?

A

Abo is larger in young
Growth of the reticulorumen and omasum = more roughage = fermentation

57
Q

What are the oligosaccharides?

A

Disaccharides
Sucrose
Lactose
Maltose
Cellbiose

58
Q

What is the function of glucan?

A

Storage and structure (starch, glycogen, cellulose)

59
Q

What is dextrin?

A

Glucan that is the intermediate in the hydrolysis of starch and glycogen

60
Q

What are the different types of glycans?

A

Heteroglycan = high molecular weight mix of sugars (hemicellulose)
Homoglycans= high molecular weight by no sugar reactions

61
Q

How is fat digested in the rumen?

A

Rumen hydrolyses fat = mored saturated
Occurs mainly in the abomasum

62
Q

Why should calcium fatty acids be administered when giving ruminants high fat content?

A

§Fat depresses the microbial activity
Long chain fatty acids cannot be absorbed in the rumen

63
Q

How is undegradable protein digested?

A

Not in the rumen
Travels to the abomasum and small intestine

64
Q

How is degradable protein digested?

A

Protein -> peptides -> amino acids -> ammonia
Ammonia is either excreted by liver or used to make microbial proteins from urea
Urea is used in the salivary glands

65
Q

Why does good quality protein need to be protected?

A

Should be protected by lipid micelles or needs to be undegradable
Rumen makes poor quality protein or non nitroprotein better

66
Q

How does the rumen digest non nitrogen protein better?

A

non protein nitrogen is made better as microbiome uses ammonia so this can be used to create VFAs

67
Q

Microbial crude protein synthesis is dependent on?

A

Protein and energy
protein > energy = energy limiting inc ammonia
energy > protein = limited by protein energy lost as methane

68
Q

What changes can affect the rumen?

A

Acidosis and alkalosis
Diurnal feed changes between batch
Starvation
Antibiotic therapy

69
Q

What are the clinical signs of chronic acidosis?

A

Caused by a diet that is too high in concentrate
- Suboptimal rumen function
- Reduced food intake
- Pain
- indigestion
- loose faeces
- low milk fat levels

70
Q

When is the acid buffering capacity of the rumen overwhelmed?

A

pH 6

71
Q

Compare cranial and caudal fermenters

A

cranial- large vat between oes and true stomach w microbiome. Can use protein from fermentative microbes
Caudal- Fermentation in the large intestinwe
Both extract from cellulose-
Both can utilise dietary hexose directly

72
Q

Outline the GIT of camelids

A

3 oesophageal diverticulums (C1(cran and caud), C2 and C3)
C1- 80% of gastric vol, homo ingesta
C2- liquid ingesta
C3 - elongated gastric glands and true stomach
Specialised saccules in C1 for VFA abso ( thin walled invaginations)

73
Q

What factors allow continuous fermentation?

A

Rumen temp
Filling and emptying
VFA absorption
Eructation
8 hr ruminating = saliva
input and output close together
Large surface area

74
Q

What is the role of ruminant saliva?

A

Acidifying effects of VFA buffered by bicarbonate and phosphate in large volumes of saliva

75
Q

How is the rumen able to be a continuous culture system?

A

Complex polysaccharides each
Microbial fermentation = VFA, gases
VFA absorbed
Eructation of gases
Partially digested food-> abomasum

76
Q

What is the role of the keratinised epiuthelium?

A

Protective
absorptive function
non glandular
Found in the rumen, reticulum and omasum

77
Q

What can be seen histologically in the reticulum?

A

Mucosa- series of cells w smaller cells inside, no conical papillae,keratinised
Reticular crest
Muscularis mucosa
Lamina propria (submucosa)
Reticular papillae

78
Q

Protozoa within the ruminant?

A

Single celled eukaryotes
Not sure on the role
100 species

79
Q

Fungi within the rumen?

A

Strict anaerobes
Colonise plant fragments
actively ferment cellulose and soluble sugars = acetate, lactate, ethanol and succinate
Fibre digestion

80
Q

What is the main bacterial pathogen in the monogastric stomach?

A

helicobacter pyori

81
Q

What is the action of helicobacter pylori?

A
  1. Into mucous layer and binds to membrane associated lipids of epithelium
  2. secretes lots of urease which neutralises => ammonia
  3. ammonia = neutral gastric acid
  4. Ammonia is toxic to epithelial cells
  5. Helicobacter can survive in higher pH
  6. Helicobacter releases protease, catalase and phospholipase = damages epithelial cells
82
Q

Properties of helicobacter pylori

A

Helical shape
Gram negative
gastric mucosa of dogs and cats
Can be determined w faecal PCR, urea breath, blood test of serology

83
Q

What factors affect protection of the monogastric stomach?

A

Age = pH
Neonates= overgrowth
Food type affects barrier function
Pharmacology

84
Q

What is assessed in ruminocentises?

A

Colour
Smell
pH - 6.7 norm
Bacterial viability
Protozoa
Sedimentation

85
Q

How to carry out ruminocentesi?

A

5 ml anaesthetic
5 mins
Clean left side 2-10cm caudal to last rib and level w stiff
16 gauge 4 inch 20 ml syringe
Aspirate fluid

86
Q

What agents cause Johnes?

A
  • Mycobacterium avium subspecies paratuberculosis
  • Gram-positive bacteria
  • aerobic and slow growing
  • acid-fast due to thick waxy wall
  • can survive pasteurisation
  • Obligate intracellular bacteria
87
Q

How is MAP spread with Johnes?

A

Faeco orally

88
Q

Johnes- How does MAP enter the host?

A

MAP=> SI => macrophages and lives in them
Early on it is contained bc slow growing
Some macrophages have apoptosis so MAP is released in the intestines
Th1 cells detect through interferrin gamma
MAP contain within GIT and GALT but not killed
Th1 cells stimulated
Lymphocytes and macrophages => submucosa

89
Q

Compare the action of Th1 and Th2 in johnes?

A

Th1 = cytokines IFNy with macrophage dominance
Th2= Cytokines IL-4, IL-10 and antibody production

90
Q

What are the stages of johnes?

A

Slow proliferation: of MAP in macrophages and in submucosa ( no antibody response, low shedding)

Increase in MAP conc in submucosal, Granulomatous inflammation: and shedding of MAP

Inflammatory response: blunts villus cells of SI
Th1-> Th2 = antibody response

V high antibody levels: and MAP shedding in faeces