Ruminant digestion and metabolism Flashcards

1
Q

What does herbivore fermentation reliant on to digest cellulose and other plant material?

A
  • micro-organisms within the GIT
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2
Q

What species use mainly foregut fermentation?

A
  • ruminants
  • hippopotami
  • camelids
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3
Q

What species use mainly hindgut fermentation?

A
  • horses
  • rabbits
  • elephants
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4
Q

How long does fermentation take?

A
  • takes a long time with slow passage and high volume
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5
Q

Herbivore fermentation relies on a constant environment - what makes the constant environment?

A
  • continuous food intake, matched with the outflow - break in this can lead to issues
  • pH regulation (bicarbonate in saliva) - 200 L saliva
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6
Q

What are the three phases in cellulose degradation?

A
  1. complex sugars are converted to simple sugars by extracellular microbial enzymes
  2. simple sugars are converted to pyruvate by intracellular microbial enzymes (through glycolysis)
  3. pyruvate converted by intracellular microbial enzymes to
    - volatile fatty acids
    - gases
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7
Q

Pyruvate is converted by intracellular microbial enzymes to volatile fatty acids - what are the VFAs and describe them?

A
  • Acetate (60-70%) - increases with roughage - 2 carbon
  • Propionate (15-20%) - increases with concentrates - 3 carbon
  • butyrate (10-15%) - 4 carbon
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8
Q

Pyruvate can be converted by intracellular microbial enzymes to gases - what are these gases and how much gas can a cow produce an hour?

A
  • carbon dioxide (CO2)
  • Methane (CH4)
  • up to 30L/hr/cow
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9
Q

What is the underlying cause for primary ketosis?

A
  • cause is usually nutritional
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10
Q

What is primary ketosis?

A
  • unable to take in enough metabolizable energy to meet metabolic demand
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11
Q

Describe primary ketosis in pregnant cows and how it can be corrected:

A
  • rumen becomes smaller due to calf taking up room = negative energy balance
  • can increase amount of concentrate, increasing the amount of propionate and therefore glucose
  • more cows would go down with this type of ketosis
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12
Q

What can lead to secondary ketosis?

A
  • another disease / anything that reduces feed intake
  • depression
  • lethargy
  • mastitis
  • metritis
  • lameness
  • LDA
  • bullying
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13
Q

What is the pattern for secondary ketosis that can aid in diagnosis?

A
  • usually sporadic and can be pinpointed to something else other than diet
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14
Q

What is pregnancy toxaemia or twin lamb disease?

A
  • sheep with multiples = shrink rumen - cant take in enough energy to lead to growth, sheep uses own reserve to feed lamb
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15
Q

What does pregnancy toxaemia cause an increased demand for?

A
  • increased demand for glucose but due to multiple foetuses drawing on glucose across the placenta
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16
Q

What is the solution to pregnancy toxaemia?

A
  • boost glucose intake
  • caesarean
  • prevention is better than treatment
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17
Q

Is all dietary protein digested in the rumen?

A
  • no some of the dietary protein passes through the rumen and is digested in the abomasum and small intestine
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18
Q

How can ammonia be used by rumen microbes?

A
  • ammonia can be used by the rumen microbes to make new amino acids which also become part of microbial protein
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19
Q

Other protein is digested into amino acids in the rumen - what can these do?

A
  • incorporated into microbes
  • deaminated (taking the amino off) generating VFAs and Ammonia
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20
Q

What can be used by the ruminal microbes to manufacture amino acids?

A
  • non-proteinaceous nitrogen (urea)
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21
Q

What happens when microbes pass through the rumen into the rest of the GIT?

A
  • digested enzymatically releasing amino acids which are absorbed into the body
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22
Q

By utilising urea and microbes what can ruminants therefore do?

A
  • can make their own essential amino acids and thrive on a low protein/poor quality protein diet
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23
Q

What helps to manufacture vitamins that can be absorbed in the small intestine?

A
  • microbes
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24
Q

What is the difference between fore and hind gut digestion processes?

A
  • Fore - ingesta leaves the rumen and enters abomasum (=monogastric stomach) and intestines, digested and absorbed similar to monogastric
  • whereas hind fermentation occurs after conventional digestion so limited absorption of fermentation products
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25
Q

What are fermentation products?

A
  • VFAs
  • microbial protein
  • vitamins
26
Q

In hindgut fermenters what cannot be utilised as well when compared to foregut fermenters?

A
  • cannot use microbial protein as there is no way of absorbing this is LI
  • vitamins (not fat soluble)
27
Q

In hindgut fermenters what is the alternative way to absorb VFA’s?

A
  • VFA merge with cell wall and can be absorbed that way
28
Q

What type of diet do hindgut fermenters need in comparison with foregut extensively managed ruminants?

A
  • need a higher quality diet in comparison
29
Q

What does bloat normally look like?

A
  • abnormally enlarged rumen or ruminal tympany
30
Q

Were does bloat usually start and how does it progress?

A
  • usually starts in the left paralumbar fossa as this is where the gas cap sits
  • progresses to ventral distention
  • then right sided distension = squishing
31
Q

What are the two types of bloat?

A
  1. free gas bloat
  2. frothy bloat
32
Q

What is free gas bloat?

A
  • anything that prevents eructation of gas
33
Q

What is frothy bloat?

A
  • gas forms a stable foam, small bubbles so cannot eructate
34
Q

In free gas bloat what causes the prevention of eructation and what can this look like?

A
  • recumbent cow or lateral recumbency
  • oesophagus is below fluid level so cannot eructate
  • fluid blocks cardia so cannot eructate
35
Q

In free gas bloat what can cause the physical obstruction to the oesophagus?

A
  • actinomyces Bovis lumpy jaw
36
Q

What can cause free gas bloat?

A
  • lack of motility in the rumen/reticulum
  • tetanus
  • hypocalcaemia
  • rumen acidosis
  • damage to vagus nerve (vagal indigestion)
37
Q

What causes frothy bloat?

A
  • bubbles of gas coalescence that doesn’t from a proper gas bubble
38
Q

In frothy bloat - grain overload/ feedlot bloat can be a cause - what is this?

A
  • high level grain diets
  • also associated with rumen acidosis
  • finely ground grains more likely
39
Q

What can grain overload sometimes cause?

A
  • free gas bloat
40
Q

pasture bloat (leguminous bloat) can also be a cause of frothy bloat - what forages can cause this?

A
  • soluble protein in some forages causes foaming
  • lush pastures
  • clovers
  • alfalfa
41
Q

How can you treat free gas bloat?

A
  • release the gas by passing a stomach tube to push obstruction through
  • or pass trocar and cannula into the rumen via the left paralumbar fossa
42
Q

What treatments are NOT successful for frothy bloat?

A
  • stomach tube or trocar and cannula unsuccessful
  • very small amount of froth released and rumen distention is NOT relived
43
Q

What treatment can be used to treat frothy bloat?

A
  • anti-foaming agents = release surface tension allowing gas bubbles to coalesce and gas can then be eructated
44
Q

How can bloat be prevented?

A
  • pasture management
  • do not feed finely ground cereals
  • at least 40% forage in the diet
45
Q

How can bloat cause internal damage?

A
  • everything gets displaces
  • starts to push diaphragm and puts pressure in the aorta
46
Q

What is LDA?

A
  • displacement of the gas-filled, distended abomasum to the left side of the abomasum, trapping it between the rumen and the abdominal wall
47
Q

What is a RDA?

A
  • displacement of the gas -filled, distended abomasum from the ventral abdominal wall into the craniodorsal right abdominal cavity
48
Q

What is an abomasal volvulus (torsion)?

A
  • displacement of the gas filled, distended abomasum from the ventral abdominal wall into the craniodorsal right abdominal cavity, secondarily creating a volvulus by vertical and horizontal rotation (abomasum, wrapped in the greater omentum) leading to a risk of necrosis
49
Q

What can cause LDA or RDA?

A
  • cow has decreased feed intake
  • energy deficient
  • ketone levels in the blood rise
  • ketosis
50
Q

What is ketosis?

A
  • build-up of ketone bodies in the blood
51
Q

What causes ketosis?

A
  • caused by a negative energy balance and fat loss (loss of BCS) which produces ketones
52
Q

What do ketones do to the cow?

A
  • makes the cow feel unwell, so she eats even less
53
Q

How can you diagnose ketosis?

A
  • high levels of ketone bodies in the blood or urine
  • beta-hydroxybutyrate
54
Q

What is the difference between primary and secondary ketosis?

A
  • Primary = underlying cause is usually nutritional
  • secondary = due to another disease
55
Q

What does fatty liver result from?

A
  • results from a state if negative energy balance one of the most important metabolic diseases of post parturient dairy cows
56
Q

When does fatty liver usually develop?

A
  • before and during parturition
57
Q

What contributes to the development of fatty liver?

A
  • periparturient depression of feed intake and endocrine changes associated with parturition and lactogenesis contribute to the development of fatty liver
58
Q

What cows are at a higher risk of fatty liver?

A
  • cows that are over conditioned at calving are at higher risk
59
Q

What causes the development of fat within liver tissues?

A
  • due to the NEFA’s being processed here and there is too much FA because the body cannot shift where it has to go
60
Q

What is fat cow syndrome a combination of?

A
  • metabolic, digestive, infectious and reproductive conditions which affect the obese periparturient cow
61
Q

What are clinical signs of fat cow syndrome?

A
  • depression
  • anorexia
  • ketonuria
62
Q

How can you prevent fat cow syndrome?

A
  • feeding a balanced diet