Metabolic Disease

Question 1

What are the clinical and subclinical levels of ketone bodies in ketosis?

Answer 1

Clinical: _>_3.0mmol/L

Subclinical: > 1.0-1.4mmol/L

Question 2

When is the transition in dairy cows relative to parturition/calving?

Answer 2

3 weeks

Question 3

Which VFAs produced by fermentation are ketogenic? What about glucogenic?

Answer 3

Ketogenic {transformed in ketone bodies}: acetate & butyrate

Glucogenic {transformed in glucose}: propionate

Question 4

What type of ketosis results from excess ketogenic VFAs in silage?

Answer 4

Alimentary ketosis
{excessive butyrate in silage}

Question 5

What are the 3 main overarching features of Ketosis?

Answer 5

1. Hypoglycemia
2. High Non-esterified Fatty Acids {NEFA}
3. Ketonemia/ketonuria

• acetoacetic acid
• acetone
• ß-hydroxybuterate

Question 6

What hormonal responses might we see in negative energy balance?

Answer 6

Glucagon,
GH,
Cortisol,
& Catecholamines
all increase…

insulin decreases…

Question 7

How do we diagnose ketosis?

Answer 7

• Ketones in blood
• serum ß-hydroxybutyrate (BHBA):
• *clinical**—>2.5-3mmol/L; subclinical—> _>_1.0-1.4mmol/L
• crude acetoacetate measurement on Ketostix or tablets
• ketones in milk
• Ketolac strips measure* BHBA;
• Pink strips measure* Acetoacetate
• GOLD STANDARD: Precision Extra {measures BHBA; more stable}

Question 8

With regard to herd management, body condition scores >4 increase the risk of what?

Answer 8

Fatty liver

Question 9

What percentage of liver weight may build up as lipids {in extreme/severe cases}?

Answer 9

12-25%

Question 10

What other periparturient dz may be risk factors {secondary to a decreased appetite} for Hepatic Lipidosis?

Answer 10

• RFM {RP}
• Metritis
• DA
• Mastitis
• Nutritional imbalances

Question 11

General pathophysiology of lipids in relation to Hepatic Lipidosis…

Answer 11

XS fatty acids {FAs} released from adipose tissue → GH; Glucagon; catecholamine stim → Hormone Sensitive Lipase {HSL} steroids

blood nonesterified FA levels rise

liver is overwhelmed & FAs are converted back to triglycerides {TG}

Question 12

How do we diagnose fatty liver?

Answer 12

UltraSound!

liver: 12.-6. ICS right
​gall bladder: 11./10. ICS right

transducer

• convex: 5MHz
• sector: 3.5MHz

Question 13

Describe the technique for performing a liver biopsy w/standard Tru-Cut® Instrument…

Answer 13

• Dorsal-ventral*—> identify top third;
• count* last ribs—> last 3rd rib space {b/t ICS 10 & 11}

Question 14

How do we make a clinical diagnosis for fatty liver?

Answer 14

• History of chronic unresponsive ketosis
• transition cow
• long dry period
• severe weight loss
• drier manure than pen mates
• drop in milk production
• weak, depressed {maybe}
• other fresh cow dz

ideally, we are trying to diagnose by combining these signs and US

Question 15

How can we attempt to establish a positive energy balance in treating HA?

Answer 15

• offer a variety of different feeds
• Orogastric intubation
• {alfalfa meal slurries, electrolytes PO, propylene glycol (glucose precursor)}
• Transfaunation
• Dextrose 50% 500mL SID/BID OR 5% infusion
  {ADD insulin —> 200 IU SQ 24-36 hrs}
• electrolytes IV
• vit-B complex & Ca2+/Mg2+
• Dexamethasone {once: 10-20mg}
• Abx if w.infectious dz
  {metritis RP, lame, mastitis}

Question 16

Why is Milk Fever considered the Gateway Dz?

Answer 16

• reduces muscle function
  
  • mastitis, DAs, metritis
• reduces feed intake
  
  • ketosis/fatty liver, DA
• reduces immune function
  
  • mastitis, RFM, metritis

Question 17

What is the magic number that blood caclium concentration should not drop below, before affecting normal function of uterus, abomasum, & rumen {w.out causing paresis}?

Answer 17

7.5mg/dL

this is referred to as subclinical hypocalcemia
& has been associated w.various periparturient disorders

Question 18

What are the 2 main results of compromised immune function d/t Hypocalcemia {sub-/clinical}

Answer 18

1. dec milk yield
2. dec. fertility

Question 19

What does PTH do?

Answer 19

released in response to low Ca2+

→ inhibits w.n**ormal or inc. Ca2+

→ activates Vit.D3
{​inc. intestinal Ca2+ absorption}

→ stims osteoclasts
{inc. uptake of Ca2+ from bone}

→ enhances renal tubular resorption &
reduces renal excretion of Ca2+

Question 20

What are some potential reasons for Jersey breeds having risk & predisposing factors over say, breeds like Holsteins??

Answer 20

More Ca2+ in colostrum
&
Less intestinal vit.D3 receptors

Question 21

How does hypomagnesemia play a role in the pathogenesis of hypocalcemia?

Answer 21

by impairing the release of PTH
& the interaction b/t PTH & target organs…

Question 22

How does hypophosphatemia play a role in the pathogenesis of hypocalcemia?

Answer 22

interferes w.activation of vit.D
by inhibiting activity of renal 1-hydroxylase enzyme

Question 23

How does blood acid-base status affect Ca2+ homeostasis?

Answer 23

alkaline blood pH lowers Ca2+ mobilization

• dietary +DCAD favors alkalosis* {hi K+/Na+ in forage of dry cow diet}
• *(Na + K) — (Cl + S)**

→ inc. bound Ca2+ from ionized pool → less efficient intestinal absorption → dec. osteoclast receptor affinity for PTH

Question 24

What’s the difference b/t stage 1 & stage 2 hypocalcemia?

Answer 24

STAGE 1
usu.standing, reduced ruminal function
{subclinical}

• *STAGE** 2
• recumbent* {sternal}; bend neck; bloating; cold extremities

Question 25

What therapy should be considered for clinical hypocalcemia {Milk Fever}?

Answer 25

immediate parenteral {IV} Calcium

Question 26

What is the dietary preventative protocol for Clinical Milk Fever?

Answer 26

DCAD:

• ​roughages low in Na+ & K+ {difficult}
• add ammonium chloride last few weeks before parturition
  {start w.25g—inc.to 100g/day}
• —5 to —10mEq/100g of DM

Question 27

What are the high risk groups for hypomagnesemia?

Answer 27

• dairy cattle first 2 months lactation
  {hi Mg2+ demand}
• beef on fertilized lush pasture
• rapid growing calves on milk diet
• stress induced {transport tetany} → cattle, sheep