Metabolic Disease Flashcards
What metabolic diseases develop from high sanitary levels/high plain of nutrition?
Ketosis
Fatty liver
Milk fever
What is ketosis?
Excess levels of circulating ketone bodies
Treatment of ketosis?
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
What are the volatile fatty acids produced by fermentation?
Acetate
Propionate
Butyrate
Which volatile fatty acids produced by fermentation of glucogenic and which are ketogenic?
Glucogenic — propionate
Ketogenic — acetate and butyrate
What is the main energy supply in ruminants ?
Glucose from gluconeogenesis
50% proprionic acid
10% glucogenic aa
10% lactate
10% glycerol
20% glucose from small bowel digestion
What is the pathophysiology of a negative energy balance leading to ketosis.?
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)
Most common cause of ketosis?
Negative energy balance
High every utilization
Eg milk production (lactose) —> 1.8kg glucose for 40kg milk produced
What are causes of a negative energy balance?
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)
What are the main features of biochem profile that you would see during a ketosis?
Hypoglycemia
High NEFA
Ketonemia/ketonuria
— acetoacetic acid
—acetone
—B-hydroxybuterate
What hormonal responses occur due to a negative energy balance?
Insulin decreases (due to low glucose)
Glucagon increases (no glycogen breakdown)
Growth hormone increases
Cortisol increase
Catecholamines (epinephrine) increases
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
True
Clinical signs associated with ketosis?
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
What is the normal level of B hydroxybutyrate in serum?
<1.0 mmol/L
Clinical ketosis occurs when B hdroxybutyrate is > ____________
2.5 to 3 mmol/L
At what levels on BHBA do you have a subclinical ketosis?
> 1.0 mmol/L to 2.5mmol/L
Ketolac strips measure ______
BHBA
Pink strips measure _________
Acetoacetate
What is the gold standard for diagnosis of ketosis?
Precision extra strips
Because BHBA is more stable
Treatment of ketosis
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
Fatty liver is a metabolic disease of __________ cows
Transition
Prevalence of fatty liver disease increases by ____% immediately after calving
50
What are the categories of fatty liver disease?
Mild (1-5% weight is TAG) centriolobular TAG infiltration
Moderate (5-10%) TAG infiltration throughout liver
Severe (10%) enlarged and necrotic
Risk factors for fatty liver disease?
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
What is the pathophysiology of hepatic lipidosis?
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
How are fats exported out of the liver?
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
What is the structure of a VLDL?
Core of TG and cholesterol
Outer coat of phospholipid
To ultrasound the liver, where should you put your probe?
Right 6th-12th ICS
Gallbladder — 10th/11th ICS
T/F: Normal liver tissue is more echogenic than renal parenchyma
True
Common biochemical abnormalites caused by hepatic lipidosis?
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)
What are the landmarks for taking a liver biopsy ?
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
What are the usually findings on a liver biopsy of a cow with hepatic lipidosis?
Triglyceride content exceeds 20% wet weight
Floats in formalin if >34%
Histopath —> vacuolated
General signalment and appearance of cows with hepatic lipidosis?
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
Treatment of hepatic lipidosis?
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
What affects can milk fever have that leads to other diseases ?
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
Reduction of blood calcium below ________ affects normal function of the uterus, abomasum, and rumen without causing paresis
- 5mg/dl
* subclinical hypocalcemia
Up to ___% of cows at calving has blood calcium <7.5mg/dL
50
What is involved in calcium homeostasis?
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+
How does Vit D actively transport Ca into the body?
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
What are risk/predisposing factors to milk fever?
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
How can hypomagnesemia and hypophoshatemia contribute to milk fever?
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
_________ blood pH lowers Ca mobilization
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
How does an alkaline blood pH lower Ca mobilization?
Increase bound Ca from ionized pool
Less efficient intestinal absorption
Decrease osteoclasts receptor affinity for PTH
How does an acidic diet increase blood Ca?
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
Clinical signs of milk fever ?
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
What are the 3 stages of milk fever?
Stage 1 — standing but reduced ruminal fxn
Stage 2– recumbency. Bend neck, cold extremities
Stage 3– comatose and unresponsive (near death)
How do you treat clinical hypocalcemia?
Immediate parenteral IV Ca therapy
— calcium gluconate (9.3%)
— calcium boroglconte (8.3%)
What rate should Ca be administered?
1g Ca/ min
Total dose = 2g/100kg BWt
Eg 10g fro 500kg cow
How can you determine if a cow is having a favorable response to Ca therapy for milk fever?
Eructation
Tremors of head and neck
HR slows down and sound increases in intensity
Attitude improves
Defecation
What is a precaution to treatment of milk fever?
Fast Ca IV infusion can cause heart failure
How can you prevent milk fever?
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)
What value do you want a DCAD diet to be to prevent milk fever?
-5 to -10
Urine pH goal = 6-7
Anionic DACD —> met acidosis —> aciduria
What is the cause of hypomagnesemia ?
How intake in feed
Occurs most commonly in nursing females and during late winter/early spring
Clinical signs associated with hypomagnesemia ?
Hyperexcitabiltiy Muscular spasms Convulsions/incoordiantion Bellowing Opisthotonos Loud heart sound Respiratory distress Collapse Death
Pastures high in what minerals can cause a hypomagnesemia due to competition for absorption?
K and Na
What cattle are high risk for hypomagnesemia
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)
Treatment for hypoMG?
200-300ml of 20% Mg sulfate IV
200ml of 50% SQ
Ca/Mg combo is best
500ml Ca borogluconate 25%
