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Animal Health and Disease > Midterm 1: Lectures 5-6 > Flashcards

Midterm 1: Lectures 5-6 Flashcards

1
Q

Metabolic disease

A

disease caused by an abnormal metabolic process
- either congenital or acquired

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2
Q

Production disease

A

encompasses diseases previously known as metabolic diseases; defined by a loss of inputs due to inputs and outputs not balancing

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3
Q

What are the most important factors of production diseases?

A
  • environment and nutrition
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4
Q

What is another name for Milk Fever?

A

Parturient paresis

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5
Q

Parturient paresis

A
  • production disease around the time of parturition
  • HYPOCALCEMIA: negative calcium balance caused by failure to mobilize reserves and by depletion of reserves to support milk production
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6
Q

What cow breed is most susceptible to parturient paresis?

A
  • Jerseys (33%); usually mature cows who are 5-10yrs old and on their 3rd-7th calf
  • other breeds are 10% susceptible (this includes beef cattle
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7
Q

What 3 stages of the lactation cycle can be affected by parturient paresis?

A
  1. 3 days pre-partum and during parturition (rare)
  2. fist 48hrs post-partum up to 10 days (majority of cases)
  3. 6-8 wks following lactation (highly susceptible cows affected)
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8
Q

During what stage of the lactation cycle are the majority of parturient paresis cases found?

A

first 48hrs post-partum up to 10 days

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9
Q

What are the 3 etiology theories for parturient paresis?

A
  1. net loss of calcium through colostrum and milk beyond capacity to absorb calcium to replenish reserves
  2. impairment to absorb calcium at the time of parturition
  3. reduced ability to absorb calcium from bone to maintain normal serum levels
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10
Q

What are the 3 stages of clinical observations seen with parturient paresis?

A
  1. brief period of hypersensitivity, tetany, restlessness, head shakes, bruxism, ataxic
  2. sternal recumbency, head kinked, drowsy, depressed, LOSS OF TETANY, ABOVE 80 BPM, weak, blank stare etc.
  3. lateral recumbency, near comatose, flaccid m, circulatory collapse, HR 120 BPM, bloat
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11
Q

How is parturient paresis treated?

A
  • Calcium borogluconate (IV) = cow will rise in minutes
  • try to place in sternal recumbency
  • add glucose, phosphorus, and Mg
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12
Q

What is the preventative treatment for parturient paresis?

A
  1. proper diet with adequate Ca2+ and increased vit D (improves uptake)
  2. high PHOSPHATE diets (decrease milk fever)
  3. change in specific ion concentration will affect incidence: potassium increases, sulfur decreases
  4. High Mg diets reduce milk fever
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13
Q

What elements affect Milk Fever?

A

Decrease incidences: phosphate, sulfur, magnesium
Increase incidences: potassium

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14
Q

What are the best ratios of calcium to phosphate to decrease parturient paresis?

A

Ca:Phosphate = 6:1 = 30% milk fever
Ca:Phosphate = 1:1 = 15% milk fever
Ca:Phosphate = 1:3 = NO milk fever

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15
Q

What is the major complication to milk fever?

A

Downer Syndrome
- animal is down for too long and end up with muscle necrosis
- even if you treat milk fever a cow with Downer won’t stand

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16
Q

What is Ketosis in ruminants?

A
  • impairment of CHO metabolism and VFA
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17
Q

How is ketosis biochemically similar in both sheep and cattle?

A
  • ketonemia, ketouria, hypoglycemia
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18
Q

How is ketosis clinically different between sheep and cattle?

A
  • Cattle = easy to treat
  • Sheep = fatal
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19
Q

Bovine ketosis

A

extreme degree of a metabolic state that is under lower levels (nutrients)
note: all high producing dairy cows in early lactation are in a negative energy balance and subclinically ketotic

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20
Q

Where is bovine ketosis most common?

A
  • 2-4 wks post-calving
  • in countries with intensive farming practices
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21
Q

How many dairy farms are affected by ketosis?

A

1-5%

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22
Q

Why does ketosis occur?

A
  • high producing heavily fed dairy cows housed in barns
  • cattle on pasture or fed poor caloric rations
  • secondary to a primary disease
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23
Q

What happens to milk production for cows that recover from ketosis?

A

They will produce less

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24
Q

Is ketosis of a high producing dairy cow in early lactation more severe than ketosis of starvation (T/F)

A

True

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25
Q

What happens to body fat stores when the body is in a negative energy balance?

A
  • moblizes fat stores to provide energy for the cow
  • too many FAs can overwhelm tissues (liver) capacity for fuel
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26
Q

What are the two types of Bovine Ketosis?

A
  1. Wasting Form
  2. Nervous Form
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27
Q

What is wasting form ketosis?

A
  • 85-87% of cases
  • decrease in appetite and milk production followed by rapid wt loss
  • KEY: milk yield falls but spontaneously recovers (but not to full potential)
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28
Q

What is nervous form of ketosis?

A
  • sudden symptoms of delirium, circling, blind, head pressing, licking, seizures; these episodes last 1-2 hrs
  • cause: hypoglycemia and ketone bodies
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29
Q

What is the difference between primary ketosis vs secondary ketosis?

A
  • Primary: dietary problem
  • Secondary: inappetence due to other causes associated with post-partuirent
30
Q

How is bovine ketosis treated?

A
  • Dextrose IV (repeated treatments)
  • oral drench of propylene glycol (good after 2-4 days of treatment)
31
Q

How can bovine ketosis be controlled?

A
  • don’t starve or over-feed at calving; provide proper ratios of calories, minerals etc.
  • daily exercise
  • rations should increase the amount of propionate produced in the rumen; monensin can increase propionate production
32
Q

What are 2 other names for Fatty Liver Complex?

A
  1. Fat cow syndrome
  2. Fatty liver disease
33
Q

What cows are affected by fatty liver complex?

A
  • beef cattle with twins prior to parturition
  • high producing dairy cattle postpartum
34
Q

Why are cows affected by fatty liver complex?

A
  • fed high grain = high energy diets
35
Q

What is the pathogenesis for fatty liver complex?

A
  1. heavy energy demands for lactation postpartum
  2. increased fat mobilization for energy demands
  3. fat accumulation in liver; cells swell with fat and become compromised
  4. fatty liver (pale)
  5. ketone bodies form, liver failure, liver enzymes elevated
36
Q

What does fatty liver complex look like?

A

“a milk fever that doesn’t respond to treatment and exclude other causes like Downer Cow”

37
Q

How is fatty liver complex treated?

A
  • Anorexic = death
  • Partially eating = supportive therapy; iv fluid + glucose, rumen juice to stimulate
38
Q

How is fatty liver complex controlled?

A
  • prevention is the best policy
  • exercise
  • individual feed rations
  • balanced diet
39
Q

What is another name for Ruminal Tympany?

A

Bloat

40
Q

Primary ruminal tympany

A
  • frothy bloat (dietary origin)
  • pasture bloat vs feedlot/grain bloat
41
Q

Secondary ruminal tympany

A
  • free gas bloat
  • physical or physiological interference with eructation
42
Q

What is the most common cause of sudden death in cattle?

A

Ruminal tympany

43
Q

within how many minutes of feeding can bloating distension occur?

A

15 minutes

44
Q

Eructation

A
  • process by which gas from forestomach is removed by way of the esophagus to the pharynx
  • mechanorecptors in dorsal sac of rumen and cardia sense gas pressure
45
Q

What is the mechanism of eructation

A
  1. rumen contracts to move gas bubble forward
  2. reticulum releases
  3. cardia opens
  4. gas is released and most is inspired by lungs
46
Q

What prevents eructation?

A

interference with sensing free gas build up in rumen or cardia

47
Q

What are the 2 types of ruminal contractions?

A
  1. primary contractions
  2. secondary contractions
48
Q

Primary contractions

A

reticulum to rumen; mixing phase

49
Q

Secondary contractions

A

rumen only; eructation phase

50
Q

Secondary Ruminal Tympany

A

= Free gas bloat
- physical obstruction preventing eructation or interference with nerve pathways (injury to vagal nerve or central processing centers)
- metabolic derangements: hypocalcemia, acidosis

51
Q

Primary ruminal tympany: pasture bloat

A
  • cows on pasture eating rich plants (rich in cytoplasmic protein); rapid digestion of these plants releases their proteins which act as ‘frothing agents’ forming many tiny gas bubbles
  • only big bubbles trigger mechanoreceptors
52
Q

When does primary ruminal tympany pasture bloat most often occur?

A

seasonal- spring and autumn

53
Q

What plants are the worse for bloat potential?

A

alfalfa>landio>red clover> subterranean clovers

54
Q

Why do animals bloat in feed lots (since it’s a relatively controlled enviro)?

A

try to maximize performance and efficiency using dietary and management strategies that can lead to GIT distrubances
- happens in FINISHING cows

55
Q

What are feedlot diets?

A

90% cereal grain + 10% forage
- greater energy density, easy to transport, custom grain blend

56
Q

Why is the high cereal grain content fed in feedlots an issue?

A

Cattle evolved on grazing forage on temperate grasslands so addition of cereal grains is novel and high energy
- for high energy grains microbial fermentation changes from slow to rapid (to digest starch)
- bacteria grow rapidly in energy rich diets

57
Q

What is a classic indication of bloat?

A

-Bloat line; found at top of the chest

58
Q

Why does bloat lead to death if untreated?

A

respiratory and cardiovascular failure (think of the bloat line)

59
Q

How is secondary bloat treated?

A
  • remove problem; if chronic problem then slaughter
60
Q

How is primary bloat treated?

A

puncture or place stomach tube to degas
- PREVENTION IS THE BEST TREATMENT

61
Q

What is the best treatment for bloat?

A

Prevention!
- alter cereal grain content in finishing diet and don’t place on green pastures
- don’t make feed too fine (bacteria can ferment)
- more forage to reduce fermentation and increase salvation
- add ionophores

62
Q

Acidosis in ruminants

A
  • a decrease in the alkali in body fluids relative to acid content
  • not one diesease rather a continuum of change
  • either acute or chronic
63
Q

What is acute acidosis defined by?

A
  • rumen pH 4-5
  • increase in gram positive bacteria, decrease in gram negative
  • rapid increase in lactic acid
  • rumen stasis, dehydration, coma, death
64
Q

Chronic acidosis

A
  • most prevalent of rumen acidosis
  • often only sign of illness is a decrease in food intake
65
Q

Reaction 1-2 during acidosis

A
  • increase starch = increase [glucose] in rumen
66
Q

Reaction 3,4,5 during acidosis

A

increase pyruvate will increase substrate for increased lactation and pH drops

67
Q

Reaction 6 during acidosis

A
  • drop in ruminal pH = Injury to rumen, reticulum, omasum
68
Q

Polioencephalomalacia

A
  • increases with rumen acidosis
69
Q

Reaction 7 to 12 of acidosis

A
  1. increase in osmolality withdraws lots of water from blood
  2. absorption of fermentation products in intestine also withdraws lots of water from blood
  3. blood pH DROPS = sever acidosis
  4. increase blood osmolity; associated with laminitis
    11/12. exretion
70
Q

What cattle are affected by acidosis?

A
  • those that consume excessive readily digestible CHOs especially grain
71
Q

Within 2-6hrs of acidosis what happens?

A
  • microbial population of rumen changes to gram positive bacteria which results in production of lactic acid
  • rumen pH falls below 5 and rumen motility ceases
  • lactic acid causes chemical rumenitis
72
Q

Prevention/treatment of acidosis

A
  • decrease rate of introducing grain
  • increase roughase
  • ionophores
  • buffers to feed

Animal Health and Disease (21 decks)

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