Macromineral disorders in dairy cattle Flashcards

1
Q

Both Milk fever and grass tetany are characterised as

A

decreased levels of blood Ca and Mg together with clinical signs.

Hence, the therapy of these diseases is intravenous infusion of calcium in milk fever and magnesium in grass tetany.

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2
Q

magnesium homeostasis is mainly
regulated by (2)

A

the absorption rate of Mg from rumen and the excretion rate through kidneys.

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3
Q

the most typical clinical
sign of milk fever is?
whereas during grass tetany the cow has?

A

the most typical clinical sign of milk fever is paresis, whereas during grass tetany cow has muscle tremors.

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4
Q

When does Milk fever usually occur?

A

Milk fever occurs usually 1 day before – 1-2 days after parturition.

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5
Q

Dairy cows will secrete ? g of calcium in the production of colostrum and milk in the early stages of lactation.

A

Dairy cows will secrete 20–30 g of calcium in the production of colostrum and milk in the early stages of lactation.

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6
Q

What stimulates PTH?
& What does PTH stimulate?
What does vit D do?

A

decreased blood concentration of Ca+ stimulates PTH

PTH in turn stimulates
- Ca release from bones (osteoclast activity), - kidney reabsorption (increases phosphate
excretion)
- activates vit D (cholecalciferol) into active calcitriol in kidneys

vit D3/calcitriol increases Ca and Phos absorption from the GI tract,
promotes renal resorption of Ca+

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7
Q

what infections can cause secondary milk fever?

A

during mastitis and severe endotoxemia, the calcium pathways are modified and hypocalcemia and paresis can occur

even severe diarrhea can also cause this due to a lack of Ca+ absorption in diarrhea.

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8
Q

Why do some cattle not respond to PTH around the onset of lactation?

A

When dry cow feeding management is off-balance, and the diet contains a lot of K+.

High K levels in the diet expose dairy cows to metabolic alkalosis, which alters the conformation of PTH receptors leading to tissues less sensitive to this hormone.

(cations (primarily K and Na) are alkalinizing because they are positively charged ions, when they are absorbed and metabolized, they tend to raise the pH of the blood, making it more alkaline.)

Under normal conditions (blood pH 7.35), in response to hypocalcemia, PTH is released and successfully works.

Under alkalotic conditions (blood pH ≥ 7.45), the shape of PTH receptors change.

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9
Q

Why does K+ in feed cause a metabolic alkalosis?

A

cations (primarily K and Na) are alkalinizing because they are positively charged ions, when they are absorbed and metabolized, they tend to raise the pH of the blood, making it more alkaline.

Thus, feeding anions (primarily chloride [Cl] and sulphate [SO4 2]) are acidifying because they are negatively charged ions, when anions are metabolized, they tend to lower the pH of the blood, making it more acidic.

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10
Q

How is hypomagnesemia related to
hypocalcemia?

A

Severe hypomagnesemia can inhibit PTH function in response to hypocalcemia.

Moderate hypomagnesemia affectshow PTH functions.

PTH can still bind to its receptors, but it can’t initiate production of second messengers without Mg.

So, in case of hypomagnesemia, the signal from PTH receptor isn’t sent forward and there is no response to PTH hormone in the body or kidney cells.

Thus, Hypocalcemia can occur.

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11
Q

what % of all the dairy cows have mild
hypocalcemia (<8 mg/dL) 24 h post partum as a physiologic respond to high milk production?

A

50% of all the dairy cows have mild
hypocalcemia (<8 mg/dL) 24 h post partum as a physiologic respond to high milk production?

This doesn’t necessarily have to cause any
problems.

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12
Q

Why are older cows more prone to suffering from milk fever? (3)

A

3 or more parturitions-cows

the number of vit D receptors in the GI tract is decreased in older cows

Ca+ release from bones is decreased as well (just not as efficient)

the number of PTH receptors in the kidneys is decreased too

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13
Q

name 3 cow related factors predisposing to milk fever

A

age (number of lactations, 3+)
milk yield (high yielders are more prone)
breed (e.g. jerseys are more prone)

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14
Q

name 5 diseases or conditions that predispose to milk fever

A

hypomagnesemia
hypophosphatemia (phos and ca metabolism are related)

ketosis
fatty liver
endotoxemia

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15
Q

name 3 environmental factors that predispose to milk fever

A
  • Dry cow feeding strategy & management
  • Sick cow management
  • decrease K content of the diet – avoid a metabolic alkalosis
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16
Q

Effects of Subclinical hypocalcemia (min.3)

A

Hypocalcemia stimulates mobilization of body fat – increased NEFA concentrations in blood – increased risk of ketosis.

Due to ca+ involvement in muscle contraction.
- Predisposes to displaced abomasum?
- Causes decreased milk yield

+ lowers the immunity,
reduces the fertility,
increases the risk of fatty liver
and retained placenta.

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17
Q

Ruminants are more prone to hypomagnesemia than monogastric
animals.

The variation in Mg metabolism among species is mainly because of

A

anatomic and physiologic differences in digestive tracts.

Species differences in Mg metabolism are attributable to variation in both absorption efficiency of Mg from the gut and reabsorption of Mg by the kidney tubules.

Ruminants absorb Mg less efficiently than nonruminants (35% vs 70% of intake).

The rumen is the main site of absorption but Absorption from the large intestine occurs with high Mg intakes.

In nonruminants, the small intestine is the main site of absorption.

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18
Q

Maintenance of normal plasma Mg levels is
dependent on

A

continuous dietary Mg supplementation!

Mg absorption from rumen depends on the Mg concentration in the ruminal fluid and the integrity of Mg transport mechanism (Na-linked active transport).

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19
Q

What Plasma Mg level will inhibit the
secretion of Mg to urine?

A

Plasma Mg level <1.8 mg/L will inhibit the
secretion of Mg to urine.

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20
Q

the main risk factors for developing of
hypomagnesemia? (6)

A

Diet related factors such as
- low Mg content in diet (needs to be supplemented!)

  • high K content in diet (high K+ will inhibit Mg absorption from rumen)
  • high content of unsaturated fatty acids in diet (high FA inhibit Mg absorption)
  • increased rate of ingesta passage (Mg doesn’t have time to absorb adequately)
  • high ruminal pH >6.5 (inhibits Mg absorption)

Of course, reduced dry matter intake as well.

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21
Q

Milk fever stages.

A

stage 1: still ambulatory but with tremors etc.

stage 2: no longer standing, cold extremities, tachy etc.

stage 3: loss of consciousness, severe bloat, unresponsive etc.

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22
Q

Normal serum Ca?
Normal serum Mg?

A

Normal serum Ca is 8.0-10.0 mg/ dL.

Normal serum Mg is 1.8-2.4 mg/ dL

Note however, the serum Ca and Mg concentrations are individually
different – cows can develop clinical disease at very different serum
concentrations.

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23
Q

Treatment plan for milk fever:

A

Intravenous calcium infusion
 Dose 9 g / 600 kg = 1-2 g/ 100 kg

 Given slowly during 15-20 min.

 Nsaids (ketoprofen, meloxicam)

Mg is often added to Ca solutions as it protects the heart from cardiotoxic effects of Ca. arrythmias and bradycardia, if you give the Ca infusion too fast.

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24
Q

When is subcut Ca appropriate?

A

Previously used in treatment/prevention of
hypocalcemia and is an approved route for
administration on product labels.

However, absorption of Ca from subcutaneous tissue needs adequate
peripheral perfusion which is decreased in cows with hypocalcemia.

+ dehydration can worsen perfusion

Subcutaneous Ca is irritating and can cause necrosis especially, if it contains glucose – risk of abscessation.

Also only keeps the blood Ca level high for only about 6 hours.

Thus, we only give Ca intravenously!

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25
Q

Oral calcium supplements are used in the
treatment of (3)

A

subclinical hypocalcemia,
after treatment of milk fever or
as prophylactic therapy for cows in risk groups.

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26
Q

Oral Ca supplement options: (3)

A

calcium chloride
calcium propionate
calcium carbonate

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27
Q

What’s the difference between
calcium chloride
calcium propionate
calcium carbonate

A
  1. Calcium chloride
     Fast absoprtion (30 min) of 50 g bolus – high bioavailability.
     Caustic to oral and pharyngeal tissues if given uncovered and repeatedly.
     Acidic response – cow starts to use it’s own Ca stores.
  2. Calcium propionate
     Slower absorption (1 h) of 75-125 g bolus
     Less injurious to tissues
  3. Calcium carbonate
     Can’t be absorbed from acidic environments or if contractions of
    digestive tract are slow

 Does not increase blood Ca concentrations – poor bioavailability

 Alkalotic agent – keep in mind the effect for PTH

 However, is cheap – can be used in diet to meet long-term Ca needs.

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28
Q

By dosing animal with large amounts of very soluable Ca, it’s possible to..?

? g Ca per dose

Given when?

A

By dosing animal with large amounts of very soluble Ca, it’s possible to force Ca from intestines to blood by means of passive diffusion.
 Old cows
 High yielding cows in earlier lactations

 50-125 g Ca per dose

 Given (12 h before calving), at calving and 12 + 24 h later (4 times total).

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29
Q

Prevention of hypocalcemia and milk fever?

A

Previously, low Ca diet during the dry period was recommended for prevention but thats difficult and also counterintuitive since nowadays we know that an alkalotic state causes PTH resistance.

Thus, we should ensure, that metabolic alkalosis doesn’t develop by decreasing K+ in the diet.

control of hypocalcemia is not successful if diet contains more than 1.8 % of K.

Dietary cation-anion difference is the point, add anion salts to the diet so that blood pH would decrease.

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30
Q

Why are cations like K+, alkalinizing?
Why are anions like Cl-, acidifying?

A

cations like K+ and Na+ are alkalinizing because they are positively charged ions, when they are absorbed and metabolized, they tend to raise the pH of the blood, making it more alkaline.

anions like Cl- and SO42- are acidifying because they are negatively charged ions, when anions are metabolized, they tend to lower the pH of the blood, making it more acidic.

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31
Q

Major cations in cows feed: (4)

A

Na +, K +, Ca 2+, Mg 2+

32
Q

Major anions in cows feed: (4)

A

Cl -, SO42-, phosphate

33
Q

The difference between the number of cation and anion particles determines the

A

blood pH
 mEq/kg

DCAD = (mEq Na+ + mEq K+) – (mEq Cl- + mEq S-)

However, these are not only cations/anions presented in the diet, so the expression should be more complex.

34
Q

There are Fixed amounts of Ca, Mg, Na and P in the diet – so instead we can manipulate

A

the amounts of K and Cl in the diet.

There’s gonna be K+ in cow’s diets anyway - Cl- anions should be added to counteract the blood alkalinity.

The concentration of Cl required in the diet to acidify the cow is 0.5 % less than the concentration of K.

High amounts of Cl reduce DMI – palatable Cl products should be used.

35
Q

When to give the adjusted DCAD diet?

A

2 weeks before calving but not earlier as the kidneys will begin buffering and the effect is lost.

then confirm if its working by checking urine pH

36
Q

normal cow urine pH?
optimal urine pH on adjusted DCAD diet?

A

normally 7.5- 8.7

on DCAD diet pH 6.5-6.8

37
Q

heart on auscultation in grass tetany?

A

Really strong heart beat and tacchycardia

38
Q

Treatment of grass tetany:

A

IV magnesium infusion 2-3 g of Mg / cow slowly over 15-20 min.

+ Nsaids

39
Q

Are there any oral Mg products available?

A

 Oral Mg products can be used after IV treatment to maintain optimal Mg concentration or to prevent hypomagnesemia in cows in risk.

  1. Magnesium oxide 100 g PO

or

  1. 50 % Magnesium sulfate 200-400 ml PO
     More available for absorption than Mg oxide.

Oral Mg salts are unpalatable – they should be given with other palatable components (molasses etc.)

40
Q

Recommendations to prevent the
occurrence of hypomagnesemia: (4)

A

Stepwise familiarization on to new pasture

Supplement minerals

Feed analysis

Treat the cows in risk groups with oral Mg

41
Q

even After two IV Ca+ treatments for milk fever, What if the cow still doesn’t stand up aftertreatment of milk fever?

A

Other macromineral disorders are rare reasons for downer cows.

But are Usually disorders of potassium (K) and phosphorous (P).
 Hypokalemia
 Hypophosphatemia (7% of milk fever cows also need phosphate)

So next step is to evaluate for one or both of these and treat them.

42
Q

Describe Hypokalemia in cows.

A

Severe hypokalemia (< 2.5 mmol in serum) may develop, if cow is anorexic.

Lactating cows are in high risk during periods of inappetence, because K is lost in milk (1.4 g of K/L of milk).

Is a rare disorder → only consider when predisposing factors are present and the treatment of other diseases is ineffective.

43
Q

Describe Hypophosphatemia in cows.

A

The restriction of fertilizer with phosphorus containing compounds can lead to decreased intake of phosphorous in dairy cows. (too much phos is bad for soil)

7% of milk fever cows also need phosphate

44
Q

hypophosphatemia can be acute or chronic, explain

A

Chronic disease → rickets in young animals and osteomalacia in adults – the
clinical signs take years to develop.

When considering chronic hypophosphatemia → check the diet and
calculate the daily amount of Phosphate needed and check against the current intake.

45
Q

Clinical signs of either hypokalemia or hypophosphatemia?

A

Unthriftiness
Anorexia
Depression
Recumbency
Muscle weakness
Tachycardia
NB S-shaped neck! (characteristic)

46
Q

Clinical signs of hypokalemia?

A

GI stasis

Rhabdomyolysis (due to potassium’s critical role in muscle cell function, Without enough energy to maintain cellular functions, muscle fibers are damaged, leading to cell rupture and the release of muscle contents)

47
Q

Clinical signs of hypophosphatemia?

A

Intravascular hemolysis
Hemoglobinuria
Pica

48
Q

If cows’ diet contains a lot of potassium why do they get hypokalemia sometimes?

A

 Due to inappetence for any reason more than 2 days.

 Gastrointestinal stasis for any reason.

 Alkalosis (displaced abomasum)

 Renal disorders, acute renal failure

 Iatrogenic causes –Glucocorticoids
(isoflupredone/dexamethasone), diuretics (furosemide).

NB! In dairy cows with normal appetite,
hypokalemia is extremely rare!

49
Q

Why does hypophosphatemia contribute to paresis?

A

Phosphate is a part of energy-transferring molecules (ATP), therefore during
hypophosphatemia ATP molecules cannot be produced and energy is not transferred in muscle cells = paresis

50
Q

Why does hypophosphatemia cause intravascular hemolysis and hemoglobinuria?

A

In erythrocytes, lack of ATP leads to increased intracellular Na and cells
become rigid and rupture in small capillaries.

Remember the lack of ATP is because ATP-building needs phosphate too.

51
Q

Treatment of hypokalemia?

A

Oral potassium chloride 20– 30 g/100 kg → 60-120 g per cow q 12 h.

IV potassium chloride max 0.5 mEq/
kg/ hour.
 Dangerous and expensive
 risk of Arrythmias → ventricular fibrillation and death.

52
Q

Treatment of hypophosphatemia?

A

IV 6 g of P supplied by 23 g of monosodium
phosphate dissolved in 1 L saline

PO 40-60 g of P, commerical products avail.

NB! P is only absorbed from intestines,
so with rumen/abomasal problems, PO
administration of P may be pointless if the phosphate can’t reach the intestines.

Phosphorous supplementation can be a part of the treatment of the downer cows, but must be limited to the recumbent stage of the disease

53
Q

Blood test of BHB tells us what exactly?

A

the exact concentration of ketone

As opposed to cow-side tests for ketones which may not be so precise and only let you know of the presence of ketones.

54
Q

Metabolic alkalosis can induce the occurrence of hypocalcemia. What is the main cause for metabolic alkalosis?

A

high potassium level in the diet

55
Q

If the cow doesn’t stand up after the first calcium treatment,

A

second calcium infusion can be given intravenously after 6-8 h.

56
Q

Ketone bodies can be utilised as an energy source by the

A

heart and skeletal muscles and in some amount in the brain.

57
Q

Functions of extracellular calcium in the organism include (3)

A

blood clotting, muscle contractions, nerve impulse transmission

58
Q

Haemoglobinuria occurs during hypophosphatemia, because

A

because low phosphate levels lead to a reduction in red blood cell membrane stability, causing hemolysis (destruction of red blood cells), which releases hemoglobin into the bloodstream. The free hemoglobin is then filtered by the kidneys, leading to its presence in urine (hemoglobinuria).

59
Q

In older cows (three or more lactations), the risk of hypocalcemia is higher because

A

the uptake of calcium from the kidneys and intestines is reduced &
the response of bones to hypocalcemia is reduced.

60
Q

An owner calls you and complains, that he has found lesions around the mouth in some lambs in a few lambs. He took the photo and sent it to you. What is your first guess as a diagnosis?

A.
Foot and mouth disease

B.
Sheep ked

C.
Contagious pustular dermatitis (ORF)

A

The correct answer is:
Contagious pustular dermatitis (ORF)

61
Q

Phosphorous is a part of

Select one or more:

a.
ATP molecule

b.
adenosine triphosphate

c.
antioxidants

A

a.
ATP molecule

b.
adenosine triphosphate

62
Q

Which of the following diseases can cause hypocalcaemia as well?

a. interdigital phlegmon

b. endotoxemic metritis

c. Hoflund’s syndrome

A

b. endotoxemic metritis

63
Q

Calcium chloride is an oral calcium product, which is rapidly absorbed from the rumen. However, the downside of this product is

A

caustic effect to oral and pharyngeal tissues.

64
Q

Treatment of clinical hypomagnesemia includes

A

IV infusion of calcium and magnesium solution

or

IV infusion of magnesium solution and NSAID-s

65
Q

Cow has calved 5 days ago. The body temperature is 39,2 ̊C, cow has dry and pale mucous membranes. The milk in one udder quarter is yellowish and watery and the somatic cell count is increased. The heart rate is increased and the rumen motility decreased. Extremities (especially ears) are cold. Cow is recumbent. Such signs are most likely caused by

A

endotoxemic mastitis

66
Q

What is the main cause for decreased magnesium level in cows’ organism?

A

diet low in magnesium

67
Q

The main feeding strategy in preventing hypocalcemia incidences in fresh cows is

A

to keep the potassium level in the dry cow diet as low as possible.

68
Q

Calcium solutions containing phosphorous can be used in primary hypophosphatemia treatment if they…

A

if they contain phosphorous in the form of phosphate.

This is the biologically active form of phosphorous.

69
Q

Hyperthermia occurs during hypomagnesemic tetany because

A

extreme muscle contractions produce a lot of heat.

70
Q

The main body source for magnesium is…

A

There are no body sources for magnesium. If cow cannot get enough magnesium from the diet, magnesium level in the organism starts to fall in the end, because magnesium cannot be redistributed from tissues to blood.

71
Q

To prevent secondary recumbency due to ischemic necrosis and pain in the muscles, cows with milk fever should be

glucocorticoids?
NSAIDS?
Turning?
soft bedding?

A
72
Q

What could be a risk factor for development of fatty liver and ketosis?

A

Excessive body condition at parturition.

73
Q

Clinical signs of hypomagnesemia usually disappear in one hour after magnesium infusion because

A

that time is needed for normalisation of magnesium levels in the cerebrospinal fluid and brain

74
Q

Why is vitamin D important in calcium homeostasis?

A

active form of vitamin D stimulates the uptake of Ca2+ from the intestines

75
Q

Right after calving, recumbent cows with hypophosphatemia can be demerged from hypocalcemia by

A

the lack of response to calcium infusion.

76
Q

Besides of downer cow syndrome, hypophosphatemia can cause

A

post-parturient haemoglobinuria

77
Q

Hypophosphatemia may occur in hypocalcemic cows, because

A

Hypophosphatemia and hypocalcemia can occur together due to parathyroid hormone activity. If cow is hypocalcemic, PTH is secreted in increased amounts. Because phosphorous is mainly absorbed with same route as calcium from the intestines, increased PTH activity puts the calcium absorption first, leading to decreased absorption of phosphourous. Anyway, phosphorous is secreted through kidneys and in saliva, which is then not absorbed from intestines.

The correct answers are: increased secretion of parathyroid hormone increases the absorption of calcium from intestines,

phosphorous is secreted in increased amounts via kidneys, saliva and feces and

absorption of phosphorous from intestines is decreased .