Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

ruminant final > Metabolic diseases > Flashcards

Metabolic diseases Flashcards

1
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Describe the pathophysiology of ketosis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe primary vs. secondary ketosis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are risk factors for ketosis?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What clinical signs are seen in ketosis?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How is ketosis diagnosed?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How is ketosis treated?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe the pathophysiology of hepatic lipidosis

A

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%.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What clinical signs are associated with hepatic lipidosis?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What diseases commonly occur concurrently with hepatic lipidosis?

A

Displaced abomasum, metritis, mastitis, parturient paresis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How is hepatic lipidosis diagnosed?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How is hepatic lipidosis treated and prevented?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Which animals get pregnancy toxemia?

A

Small ruminants and beef cattle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are risk factors for pregnancy toxemia?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What clinical signs are associated with pregnancy toxemia?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are differential diagnoses for pregnancy toxemia?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How is pregnancy toxemia diagnosed?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How is pregnancy toxemia treated?

A

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

20
Q

Describe protein energy malnutrition

A

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.

21
Q

What are the 4 M’s of recumbent cows?

A

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

22
Q

How do PTH and vitamin D effect ionized calcium?

A

They increase it

23
Q

How does calcitonin effect ionized calcium?

A

It decreases it

24
Q

What is milk fever/periparturient paresis?

A

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

25
Q

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

A

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

26
Q

How does hypocalcemia relate to metabolic alkalosis and PTH?

A

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

27
Q

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

A

Hypersensitive nerves, irritable, weight shifting, weakness, tachycardia

28
Q

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

A

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

29
Q

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

A

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

30
Q

How is milk fever/periparturient paresis diagnosed?

A

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

31
Q

How is stage 1 milk fever/periparturient paresis treated?

A

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

32
Q

How is stage 2 milk fever/periparturient paresis treated?

A

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

33
Q

How is stage 3 milk fever/periparturient paresis treated?

A

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

34
Q

How is milk fever/periparturient paresis prevented?

A

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

35
Q

What are causes of hypophosphatemia?

A

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

36
Q

What are the clinical signs of hypophosphatemia?

A

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

37
Q

Describe the pathophysiology of post-parturient hemoglobinuria

A

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

38
Q

What are the clinical signs of post-parturient hemoglobinuria?

A

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

39
Q

How is hypophosphatemia treated?

A

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

40
Q

What are the clinical signs of hypokalemia?

A

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

41
Q

What are differentials for hypokalemia?

A

GI diseases, botulism, hypocalcemia, cervical trauma

42
Q

How is hypokalemia treated?

A

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

43
Q

How can hypokalemia be prevented?

A

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

44
Q

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

A

No; needs to be supplemented

45
Q

Describe the pathophysiology of hypomagnesemia

A

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

46
Q

What are the clinical signs associated with hyopmagnesemia?

A

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

47
Q

How is hypomagnesemia treated?

A

IV magnesium therapy +/- oral magnesium administration

ruminant final (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions