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RUSVM LAM II > Metabolic Disease > Flashcards

Metabolic Disease Flashcards

1
Q

What metabolic diseases develop from high sanitary levels/high plain of nutrition?

A

Ketosis
Fatty liver
Milk fever

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2
Q

What is ketosis?

A

Excess levels of circulating ketone bodies

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3
Q

Treatment of ketosis?

A

Urine dipstick — if moderate to large, treat with IV dextrose/oral glucose

Transfaunation if ruminal fermentation failure

Remove underlying cause

If ketosis persists suspect fatty liver disease

Transition period — 3 weeks before to 3 weeks following parturition

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4
Q

What are the volatile fatty acids produced by fermentation?

A

Acetate
Propionate
Butyrate

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5
Q

Which volatile fatty acids produced by fermentation of glucogenic and which are ketogenic?

A

Glucogenic — propionate

Ketogenic — acetate and butyrate

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6
Q

What is the main energy supply in ruminants ?

A

Glucose from gluconeogenesis

50% proprionic acid
10% glucogenic aa
10% lactate
10% glycerol

20% glucose from small bowel digestion

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7
Q

What is the pathophysiology of a negative energy balance leading to ketosis.?

A

Low glucose —> inhibits TCA cycle

Low nutrition —> excessive mobilization of amounts of volatile fatty acids
B oxidation produces Acetyl CoA which is turned into ketones (BHB, acetone, acetoacetic acid)

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8
Q

Most common cause of ketosis?

A

Negative energy balance

High every utilization
Eg milk production (lactose) —> 1.8kg glucose for 40kg milk produced

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9
Q

What are causes of a negative energy balance?

A

Insufficient energy production
— genetically high milk producers (primary ketosis)

—Reduced rumen volume (30% decrease)

—Appetite drops — estrogen suppress

—Dry cow diet — adaption to fresh cow diet
—Inadequate balanced rations
— fermentation failure (simple indigestion) -> poor forage quality
—subacute rumen acidosis
—excessive butyrate in silage (alimentary ketosis)
—Dz
— thin cow on poor diet (starvation ketosis)

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10
Q

What are the main features of biochem profile that you would see during a ketosis?

A

Hypoglycemia
High NEFA

Ketonemia/ketonuria
— acetoacetic acid
—acetone
—B-hydroxybuterate

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11
Q

What hormonal responses occur due to a negative energy balance?

A

Insulin decreases (due to low glucose)

Glucagon increases (no glycogen breakdown)

Growth hormone increases

Cortisol increase

Catecholamines (epinephrine) increases

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12
Q

T/F: fatty acids cannot be converted into glucose, but can be used to produce ATP via B oxidation within mitochondria located in the liver and muscles

A

True

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13
Q

Clinical signs associated with ketosis?

A

Nonspecific signs of reduced milk production, decreased appetite, weight loss, lower activity

Milk fat : protein

Fruity smell to breath (acetone)
Wasting ketosis —> severe weight loss

Nervous ketosis

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14
Q

What is the normal level of B hydroxybutyrate in serum?

A

<1.0 mmol/L

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15
Q

Clinical ketosis occurs when B hdroxybutyrate is > ____________

A

2.5 to 3 mmol/L

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16
Q

At what levels on BHBA do you have a subclinical ketosis?

A

> 1.0 mmol/L to 2.5mmol/L

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17
Q

Ketolac strips measure ______

A

BHBA

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18
Q

Pink strips measure _________

A

Acetoacetate

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19
Q

What is the gold standard for diagnosis of ketosis?

A

Precision extra strips

Because BHBA is more stable

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20
Q

Treatment of ketosis

A

Establish positive energy balance
—> different feeds
—> orogastric intubation (alfalfa meal slurries, electrolytes, and propylene glycol)

Transfaunation

Propylene glycol
—> converted into glucose by the liver

Intravenous glucose administration
—> continuous infusion 2.5-5% dextrose

Glucocorticoids
—> enhance gluconeogenesis and reduce milk production

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21
Q

Fatty liver is a metabolic disease of __________ cows

A

Transition

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22
Q

Prevalence of fatty liver disease increases by ____% immediately after calving

A

50

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23
Q

What are the categories of fatty liver disease?

A

Mild (1-5% weight is TAG) centriolobular TAG infiltration

Moderate (5-10%) TAG infiltration throughout liver

Severe (10%) enlarged and necrotic

24
Q

Risk factors for fatty liver disease?

A

Same as ketosis — negative energy balance

Genetic of high milk production 
Small rumen capacity 
Appetite decreased 
— hormones 
—peripartuient diseases: RFM, metritis, DA, mastitis, nutritional imbalances

Obesity BSC 4.5

25
Q

What is the pathophysiology of hepatic lipidosis?

A

Excessive amounts of fatty acids released from adipose tissues —> growth hormone, glucagon, and catecholamines stimulate hormone sensitive lipase

Blood nonesterified fatty acid (NEFA) levels rise

Liver takes up fatty acids with the aim of oxidizing and secreting —> liver is overwhelmed and fatty acids are converted back to TG

26
Q

How are fats exported out of the liver?

A

TAGS usually exported by very low density lipoproteins (VLDL)

Ruminants are not very good at this ^

So fats are slowly exported or accumulate in liver and reduce its ability for gluconeogenesis

27
Q

What is the structure of a VLDL?

A

Core of TG and cholesterol

Outer coat of phospholipid

28
Q

To ultrasound the liver, where should you put your probe?

A

Right 6th-12th ICS

Gallbladder — 10th/11th ICS

29
Q

T/F: Normal liver tissue is more echogenic than renal parenchyma

A

True

30
Q

Common biochemical abnormalites caused by hepatic lipidosis?

A

Hypoglycemia <75mg/dL

Low insulin
Elevated serum NEFA concentrations
Low serum triglycerides (VLDL)

High serum ketone concentrations (BHBA)

Elevated ammonia (waste product)

Low BUN (Blood urea N —> product of ammonia catabolism)

31
Q

What are the landmarks for taking a liver biopsy ?

A

Draw a line about 1/3 of the animals depth from the whithers to the sternum

Go caudal 3 ICS.

This takes you central in the liver

32
Q

What are the usually findings on a liver biopsy of a cow with hepatic lipidosis?

A

Triglyceride content exceeds 20% wet weight

Floats in formalin if >34%

Histopath —> vacuolated

33
Q

General signalment and appearance of cows with hepatic lipidosis?

A

Transition cow

High BCS —> high days open

History of chronic unresponsive ketosis
Long transition period

Severe weight loss
Drier manure than pen mates
Drop in milk production
Weak, depressed

34
Q

Treatment of hepatic lipidosis?

A

Establish a positive energy balance

  • dextrose 50% 500ml SID or BID or 5% infusion
  • add insulin

Electrolytes IV
Vit B complex, Ca, and Mg
Dexamethasone

And with infectious dz

35
Q

What affects can milk fever have that leads to other diseases ?

A

Reduces milk function —> more mastitis, DA, and metritis

Reduces feed intake —> ketosis/fatty liver and more displaced abomasum

Reduces immune function —> more mastitis, RFM, and metritis

36
Q

Reduction of blood calcium below ________ affects normal function of the uterus, abomasum, and rumen without causing paresis

A
  1. 5mg/dl

* subclinical hypocalcemia

37
Q

Up to ___% of cows at calving has blood calcium <7.5mg/dL

A

50

38
Q

What is involved in calcium homeostasis?

A

Parathyroid hormone released with low blood Ca levels. Inhibits with normal to increased Ca 2+ levels

—> activated vit D3 -> increased intestinal Ca2+ absorption
—> stimulates osteoclasts increasing uptake of Ca2+ from bone
—> enhance renal tubular resorption and reduces renal excretion of Ca2+

39
Q

How does Vit D actively transport Ca into the body?

A

Vit D goes from blood into cell and binds to VitD receptor—> Ca binds to protein to bring Ca into cell

Ca ATPase pumps Ca into the blood stream

40
Q

What are risk/predisposing factors to milk fever?

A

Acute Ca output in colostrum (with low influx from intestine or bone)

Milk production

Breed: jersey have more Ca in colostrum and less intestinal vit D3 receptors

> 4 lactation (older cows have higher risk) — decreased in activated VitD receptors with age and decrease osteoclasts

Blood levels of Mg, Ca and PO4

41
Q

How can hypomagnesemia and hypophoshatemia contribute to milk fever?

A

HypoMg —> impairs release of PTH and the interaction between PTH and target organs

HypoPhos —> interferes with activation of vitD by inhibiting renal 1-hydroxylase enzyme

42
Q

_________ blood pH lowers Ca mobilization

A

Alkaline

Dietary +DCAD (dietary cation-anion difference) favors alkalosis because of high K and Na in forage in the dry cow diet

(Na + K) - (Cl- + S-)
Cation - Anion

43
Q

How does an alkaline blood pH lower Ca mobilization?

A

Increase bound Ca from ionized pool

Less efficient intestinal absorption

Decrease osteoclasts receptor affinity for PTH

44
Q

How does an acidic diet increase blood Ca?

A

Increases plasma levels of activated Vit D3 increasing intestinal absorption

Causes calciuria thus increasing gPTH secretion

Increases the affinity of osteoclasts bone receptors for PTH thus facilitating the Ca mobilization from bone

Releases bound Ca into ionized

45
Q

Clinical signs of milk fever ?

A

Kink in neck
Recused jaw and tongue tone
Flaccid paralysis

Suspended rumen contraction
Reduced anal tone
Rectum full

Cold extremities (due to depressed cutaneous circulation) 
Tachycardia >100bpm

Weak corneal reflex
Semi-comatose sate

46
Q

What are the 3 stages of milk fever?

A

Stage 1 — standing but reduced ruminal fxn

Stage 2– recumbency. Bend neck, cold extremities

Stage 3– comatose and unresponsive (near death)

47
Q

How do you treat clinical hypocalcemia?

A

Immediate parenteral IV Ca therapy

— calcium gluconate (9.3%)
— calcium boroglconte (8.3%)

48
Q

What rate should Ca be administered?

A

1g Ca/ min

Total dose = 2g/100kg BWt
Eg 10g fro 500kg cow

49
Q

How can you determine if a cow is having a favorable response to Ca therapy for milk fever?

A

Eructation

Tremors of head and neck

HR slows down and sound increases in intensity

Attitude improves

Defecation

50
Q

What is a precaution to treatment of milk fever?

A

Fast Ca IV infusion can cause heart failure

51
Q

How can you prevent milk fever?

A

Ca gel at parturition

Avoid over feeding of Ca. Give maintenance PO4

Avoid over conditioning and stress

Attend to cow comfort and frequent pre and post partum observation

Supplement diet
Oral or injectable Vit D prior to calving

DACD diet — anion sources! (Eg add ammonium chloride before parturition)

52
Q

What value do you want a DCAD diet to be to prevent milk fever?

A

-5 to -10

Urine pH goal = 6-7

Anionic DACD —> met acidosis —> aciduria

53
Q

What is the cause of hypomagnesemia ?

A

How intake in feed

Occurs most commonly in nursing females and during late winter/early spring

54
Q

Clinical signs associated with hypomagnesemia ?

A 
Hyperexcitabiltiy
Muscular spasms 
Convulsions/incoordiantion 
Bellowing 
Opisthotonos 
Loud heart sound 
Respiratory distress 
Collapse 
Death
55
Q

Pastures high in what minerals can cause a hypomagnesemia due to competition for absorption?

A

K and Na

56
Q

What cattle are high risk for hypomagnesemia

A

Dairy cattle first 2 months lactation

Beef on fertilized lush pasture (high Na and K)

Rapid growing calves on milk diet

Stress induced (transport tetany)

57
Q

Treatment for hypoMG?

A

200-300ml of 20% Mg sulfate IV

200ml of 50% SQ

Ca/Mg combo is best

500ml Ca borogluconate 25%

RUSVM LAM II (22 decks)

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