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LAM II-RUSVM COPY > Metabolic Diseases FA-Bittar > Flashcards

Metabolic Diseases FA-Bittar Flashcards

1
Q

What is the most common metabolic disease in cattle?

A

Ketosis

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2
Q

When is ketosis most commonly observed?

A

Early lactation cows

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3
Q

If there is a large amount of ketones present on the urine dipstick, what should be used to treat it?

A

IV dextrose/oral glucose precursors

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4
Q

What can result from untreated ketosis?

A

Fatty liver

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5
Q

When are cows most likely to have ketosis?

A

During the transition period (3 weeks before, 3 weeks post calving)

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6
Q

What are some pathogenesis of ketosis?

A
  1. DMI and Ca decreases
  2. Milk flow increases rapidly
  3. BCS deteriorates from nutrient deficiency
  4. Negative energy balance widens. Increased fat mobilization to the liver and ketone body accumulation may occur
  5. Peak milk is approaching
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7
Q

What are the hormonal responses in ketosis?

A

Insulin decreases, glucagon increases, GH increases, cortisol increases, catecholamines increase

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8
Q

What are two main features of ketosis?

A

Hypoglycemia and high NEFA

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9
Q

What is the gold standard dx for ketosis?

A

Ketones in blood

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10
Q

What are some tx routes for a ketosis patient?

A

Establish a positive energy balance
Propylene glycol (converted to glucose by liver)
CRI IV glucose administration (2.5-5% dextrose)
Glucocorticoids (enhance gluconeogenesis and reduce milk production)

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11
Q

What BCS will we be concerned about an increased risk of fatty liver pre-partum?

A

BCS>4

We want around 3.5 at time of calving

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12
Q

What is the difference in the calorie content of a far off diet vs. close up diet?

A

Far-off diet (far from parturition) should be low in calories
Close up diet (close to parturition) should be high in calories

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13
Q

What is a risk factor for hepatic lipidosis?

A

Negative energy balance

Genetic high milk, small rumen, appetite decreased, DA, mastitis, nutritional imbalances, obesity

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14
Q

T/F: Prevention of hepatic lipidosis is often more rewarding than Tx?

A

TRUE

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15
Q

What is the pathophysiology of hepatic lipidosis?

A

Excessive amount of FA released from adipose tissues stimulating hormone sensitive lipase steroids
Blood nonesterified FA levels rise
Liver takes up FA w/ aim of oxidizing & secreting them- but overwhelmed and converted back to TG

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16
Q

How are TG transported from the liver?

A

Very low density lipoprotein

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17
Q

What does overaccumulation of TG cause in the liver?

A 
Cell swelling
Disruption of cell metabolism
Liver enzyme levels rise
Loss of hepatic function
Capsule rupture
Unable to increase VLDL synthesis
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18
Q

Where is the liver located in terms of ICS for US?

A

12-6 ICS (R)

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19
Q

Where is the gall bladder located in terms of ICS for US?

A

11-10 ICS (R)

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20
Q

What are some metabolic derangements found with fatty liver disease?

A 
Hypoglycemia
Low insulin
Elevated serum NEFA
Low TG (they are all in the liver stuck with no way out)
High serum ketone concentrations
Elevated ammonia
Low BUN
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21
Q

What is the maximum TG count that should be in the liver until it is deemed abnormal?

A

TG content shouldn’t exceed 20%

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22
Q

At what TG concentration does the liver float in formalin?

A

34%

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23
Q

What are some tx options for Fatty Liver?

A

Establish positive energy balance: offer different feeds, orogastric intubation or transfaunation
Dextrose 50% 500 mL BID or 5% infusion
Electrolytes IV
Vitamin B complex

24
Q

What is the metabolic disease of transition cows that presents as low calcium?

A

Milk fever (hypocalcemia)

25
Q

What is the normal blood Ca levels?

A

8-10 mg/dL

26
Q

When is milk fever most commonly seen?

A

-1 to +3 days postpartum

27
Q

What are three main effects of hypocalcemia?

A

Reduced muscle function
Reduced feed intake
Reduced immune function

28
Q

T/F: Due to the reduced muscle function from milk fever, DA, metritis and mastitis is commonly associated with milk fever

A

TRUE

29
Q

What is the Ca blood level that defines sub-clinical hypocalcemia?

A

<7.5 mg/dL

Affects normal function of the uterus, abomasum and rumen but doesn’t cause paresis

30
Q

What may appear before hypocalcemia in subclinical milk fever?

A

Ruminal dysfunction

31
Q

What is subclinical milk fever closely associated with?

A

Displaced abomasum

32
Q

What is the calcium homeostasis pathway?

A

PTH released when low blood Ca levels –> activates Vit D3 –> increases intestinal Ca absorption –> stimulates osteoclasts increasing uptake of Ca from bone –> enhance renal tubular resorption & reduces renal excretion of Ca

33
Q

What form of Ca is metabolically active?

A

Ionized Ca

34
Q

What are three excretion routes for Ca in the body?

A

Milk
Endogenous fecal loss
Urine

35
Q

What type of Ca transport is the more efficient method of mobilizing Ca to bloodstream?

A

Vitamin D-dependent active transport of Ca

36
Q

how much calcium must be mobilized per day?

A

30g/day to maintain energy balance

37
Q

What are predisposing factors to hypocalcemia?

A

Milk production
Jersey cattle
>4 lactations
Blood levels of Mg, Ca and PO4

38
Q

Why are Jersey’s a risk factor for milk fever?

A

More Ca in colostrum and less intestinal vitamin D receptors

39
Q

Why do older cows have a higher risk of hypocalcemia?

A

Decrease in activated vitamin D3 gut receptors with age

Decrease in osteoclasts with age

40
Q

What factor if decreased impairs the release of PTH?

A

Mg

41
Q

How does hypophosphatemia interfere with activation of vitamin D?

A

Inhibits activity of renal 1-hydroxylase enzyme

42
Q

What effect does an alkaline pH have on Ca mobilization?

A

Decreases Ca mobilization by producing less efficient intestinal absorption and decreasing osteoclast receptor affinity for PTH

43
Q

What are the ions involved in the DCAD diet?

A

Na
K
Cl
S

44
Q

What effect does an acidic pH have on Ca mobilization?

A

Increases blood Ca by:

  • increasing intestinal absorption
  • increases affinity of osteoclast bone receptors
  • Releases bound Ca into iCa
45
Q

Why do we aim for an acidic blood pH in prepartum cows to help reduce hypocalcemia?

A

This will prepare the cow for a Ca shortage so that once the calf comes she has a full potential for Ca availability

46
Q

T/F: Sub-clinical hypocalcemia causes forestomach hypomotility

A

TRUE (abomasal displacement associated with this)

47
Q

What are CS of hypocalcemia?

A

Down, flaccid paralysis, kink in the neck, reduced jaw tone, normal/subnormal temperature, cold extremities, tachycardia, weak corneal reflex

48
Q

What are the 3 stages of milk fever?

A

Stage 1: standing, reducing ruminal function, subclinical (Ca <7.5 mg/dL)
Stage 2: sternal recumbency, bend neck (S/Z shape), bloating, and cold extremities (CALL VET IN THIS STAGE) 5 mg/dL near death Ca < 5 mg/dL

49
Q

What are favorable responses of therapy?

A

Eructation, tremors, slow heart rate, attitude improves and defecation

50
Q

What rate should IV Ca be administered?

A

SLOW IV INFUSION- can lead to heart failure or death

51
Q

What is the target urine pH of a cow on the DCAD diet?

A

6-7

52
Q

T/F: Mg is absorbed in the rumen and stored throughout the body

A

False- Mg is not stored in the body

53
Q

What hormone conserves Mg levels?

A

PTH

54
Q

What is grass tetany caused by?

A

Low blood Mg

Also known as staggers

55
Q

What does low Mg cause in terms of CS?

A

Hyperexcitability, muscle spasms, convulsions, respiratory distress, collapse and death

56
Q

What are the minerals that are high and low in lush fertilized pastures?

A

High: K and N
Low: Mg

57
Q

What are high risk groups for Grass tetany?

A

Dairy cattle in first 2 months of lactation (high Mg demand)
Beef on fertilized lush pasture
Rapid growing calves on milk diet
Stress induced

LAM II-RUSVM COPY (19 decks)

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