Metabolic diseases Flashcards by Cassie Lilley

When do most metabolic problems occur in dairy cattle and why?

Around the time of calving (3 weeks before-after)
Because of the significant changes in energy demand/endocrine status/feed intake

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Describe the pathophysiology of ketosis

Negative energy balance with lack of carbohydrates -> increased fat mobilization -> increased ketone body formation

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Describe primary vs. secondary ketosis

Primary- negative energy balance in early lactation, hypoglycemia, responds well
Secondary- disease-induced inappetence +/- fatty liver in overconditioned sows, treatment often unsuccessful

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What are risk factors for ketosis?

First 6 weeks of lactation, high milk yield, higher parity, overconditioning, genetics, problems during previous transition period

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What clinical signs are seen in ketosis?

Gradual loss of appetite, decreased milk production, ruminal hypomotility, mild dehydration, dullness/depression, weight loss, altered CNS function (for nervous ketosis), normal TPR

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How is ketosis diagnosed?

Special odor to cow’s breath (subjective, not sensitive), ketones can be detected in blood (best), urine (overly sensitive), milk (low sensitivity, high specificity)

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How is ketosis treated?

Administer propylene glycol, increase dietary intake, provide IV dextrose, provide glucocorticoids, consider rumen transfaunation, ionophores, and B-vitamins

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Describe the pathophysiology of hepatic lipidosis

Rate of hepatic triglyceride formation exceeds oxidation of fatty acids and release of VLDLs, leading to storage. Liver becomes overwhelmed with fatty acids. Mortality rate can exceed 25%.

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What clinical signs are associated with hepatic lipidosis?

Depression, anorexia, weight loss, weakness, recumbency, rumen hypomotility, decreased milk production

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What diseases commonly occur concurrently with hepatic lipidosis?

Displaced abomasum, metritis, mastitis, parturient paresis

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How is hepatic lipidosis diagnosed?

Liver biopsy (gold standard), ultrasound, increased liver enzymes and NEFAs, leukopenia all suggestive but not diagnostic

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How is hepatic lipidosis treated and prevented?

Eliminate negative energy balance, treat any concurrent disease, prevent over-conditioning

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Which animals get pregnancy toxemia?

Small ruminants and beef cattle

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What is pregnancy toxemia and how does it compare to ketosis in dairy cattle?

It is ketosis associated with late pregnancy and decreased ruminal fill, it has lower morbidity and higher mortality (>50%)

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What are risk factors for pregnancy toxemia?

Ewes >2 lambs, does >3 kids, poor quality feed, over or severely under conditioned animals, stress

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What clinical signs are associated with pregnancy toxemia?

Anorexia, depression, weakness, recumbency, neurological signs, may have concurrent diseases

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What are differential diagnoses for pregnancy toxemia?

Hypocalcemia, hypomagnesemia, mastitis, enterotoxemia, listeriosis, polioencephalomalacia, anemia/parasitism, copper toxicosis

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How is pregnancy toxemia diagnosed?

Beta-hydroxybutyrate found in blood or acetoacetate found in urine, presence of multiple fetuses on ultrasound is supportive, chemistry panel with high fatty acids, metabolic acidosis, hypocalcemia/kalemia/glycemia, azotemia, increased liver enzymes

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How is pregnancy toxemia treated?

Decide if dam or kids are more important- if dam is more important, emergency c-section, if kids more important induce labor when appropraite

Describe protein energy malnutrition

Negative energy balance in pregnant beef cattle causing signs similar to pregnancy toxemia/ketosis. Prevent by making sure cows go into 3rd trimester with good BCS and by feeding high quality forage and grain.

What are the 4 M’s of recumbent cows?

Mastitis
Metritis
Musculoskeletal/neurological
Metabolic (hypocalcemia/kalemia/magnesemia/phosphatemia)

How do PTH and vitamin D effect ionized calcium?

They increase it

How does calcitonin effect ionized calcium?

It decreases it

What is milk fever/periparturient paresis?

Loss of serum calcium within 24-48 hours of calving due to lactation; compromises muscle and nerve function resulting in paralysis

What are the risk factors for milk fever/periparturient paresis?

Older age, Jerseys and Guernseys > Holsteins, high body condition, poor nutrition, high producing cow, hypomagnesemia, metabolic alkalosis, within 72 hours of parturition

How does hypocalcemia relate to metabolic alkalosis and PTH?

High potassium diet leads to metabolic alkalosis which alters conformation of PTH receptor causing decreased bone resorption and renal reabsorption and failure to make vitamin D

Describe the clinical signs of stage 1 milk fever/periparturient paresis

Hypersensitive nerves, irritable, weight shifting, weakness, tachycardia

Describe the clinical signs of stage 2 milk fever/periparturient paresis

Sternal recumbency with head tucked and neck in S-shape, flaccid paralysis, muscle fasciculations, tachycardia, decreased intensity of heart sounds, poor perfusion, mild bloat, GI stasis, urine retention, dry feces, slow PLR

Describe the clinical signs of stage 3 milk fever/periparturient paresis

Lateral recumbency with progressive loss of consciousness, severe bloat, very quiet heart sounds, severe tachycardia, coma, and eventual death

How is milk fever/periparturient paresis diagnosed?

Clinical signs and history, biochemistry or blood gas analysis showing decreased calcium

How is stage 1 milk fever/periparturient paresis treated?

Calcium borogluconate IV (23% solution), over 15 minutes, can give second bottle SQ to cover ongoing losses

How is stage 2 milk fever/periparturient paresis treated?

Oral calcium (must be careful, cow is weak and calcium is caustic so avoid aspiration) + treatment from stage 1

How is stage 3 milk fever/periparturient paresis treated?

Hobbles to keep cow sternal, offer food and water, hygiene and udder control + treatment from stage 1

How is milk fever/periparturient paresis prevented?

Use a high cation diet to create compensated metabolic acidosis, give oral calcium boluses at time of calving

What are causes of hypophosphatemia?

Decreased intestinal absorption (anorexia, parasitosis, etc.), increased renal excretion (diuresis or hypocalcemia), shift from ECS to ICS (glucose administration, refeeding syndrome)

What are the clinical signs of hypophosphatemia?

Anorexia, weight loss, reduced milk production, reduced fertility, osteomalacia, recumbency, weakness

Describe the pathophysiology of post-parturient hemoglobinuria

Severe, acute hypophosphatemia occurring in the first 4-6 weeks of lactation, leading to decreased ATP, increased osmotic fragility of RBCs, IV hemolysis, and hemoglobinuria

What are the clinical signs of post-parturient hemoglobinuria?

Depression, weakness, anorexia, drop in milk yield, hemoglobinuria, icterus

How is hypophosphatemia treated?

Restore phosphorus dietary requirements, treat hypocalcemia, provide IV phosphorus, provide blood transfusion

What are the clinical signs of hypokalemia?

Depression, recumbency, muscle tone severely reduced, tachycardia, abnormal neck posture, GI stasis, rhabdomyolysis

What are differentials for hypokalemia?

GI diseases, botulism, hypocalcemia, cervical trauma

How is hypokalemia treated?

Address any pre-existing disease, provide oral potassium supplementation or IV (oral preferred)

How can hypokalemia be prevented?

Monitor herd for anorexia or post-partum disease, use caution with mineralocorticoids

Do most forages have the required amount of magnesium in them?

No; needs to be supplemented

Describe the pathophysiology of hypomagnesemia

Lactating animals grazing on lush pastures high in potassium and nitrogen in the spring or fall develop low magnesium

What are the clinical signs associated with hyopmagnesemia?

Anorexia, nervousness, decreased milk production, hyperexcitability, tetany, convulsions, death

How is hypomagnesemia treated?

IV magnesium therapy +/- oral magnesium administration