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LAM II > Metabolic Disease > Flashcards

Metabolic Disease Flashcards

1
Q

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

A

Clinical: _>_3.0mmol/L

Subclinical: > 1.0-1.4mmol/L

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2
Q

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

A

3 weeks

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3
Q

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

A

Ketogenic {transformed in ketone bodies}: acetate & butyrate

Glucogenic {transformed in glucose}: propionate

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4
Q

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

A

Alimentary ketosis
{excessive butyrate in silage}

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5
Q

What are the 3 main overarching features of Ketosis?

A
  1. Hypoglycemia
  2. High Non-esterified Fatty Acids {NEFA}
  3. Ketonemia/ketonuria
  • acetoacetic acid
  • acetone
  • ß-hydroxybuterate
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6
Q

What hormonal responses might we see in negative energy balance?

A

Glucagon,
GH,
Cortisol,
& Catecholamines
all increase…

insulin decreases…

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7
Q

How do we diagnose ketosis?

A
  • 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}
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8
Q

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

A

Fatty liver

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9
Q

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

A

12-25%

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10
Q

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

A
  • RFM {RP}
  • Metritis
  • DA
  • Mastitis
  • Nutritional imbalances
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11
Q

General pathophysiology of lipids in relation to Hepatic Lipidosis…

A

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}

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12
Q

How do we diagnose fatty liver?

A

UltraSound!

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

transducer

  • convex: 5MHz
  • sector: 3.5MHz
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13
Q

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

A
  • Dorsal-ventral*—> identify top third;
  • count* last ribs—> last 3rd rib space {b/t ICS 10 & 11}
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14
Q

How do we make a clinical diagnosis for fatty liver?

A
  • 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

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15
Q

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

A
  • 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}
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16
Q

Why is Milk Fever considered the Gateway Dz?

A
  • reduces muscle function
    • mastitis, DAs, metritis
  • reduces feed intake
    • ketosis/fatty liver, DA
  • reduces immune function
    • mastitis, RFM, metritis
17
Q

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}?

A

7.5mg/dL

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

18
Q

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

A
  1. dec milk yield
  2. dec. fertility
19
Q

What does PTH do?

A

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+

20
Q

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

A

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

21
Q

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

A

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

22
Q

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

A

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

23
Q

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

A

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

24
Q

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

A

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

  • *STAGE** 2
  • recumbent* {sternal}; bend neck; bloating; cold extremities
25
Q

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

A

immediate parenteral {IV} Calcium

26
Q

What is the dietary preventative protocol for Clinical Milk Fever?

A

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
27
Q

What are the high risk groups for hypomagnesemia?

A
  • 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

LAM II (22 decks)

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