Macro Minerals Flashcards by Leah Arth

The four Organic Basic Elements

Hydrogen
Carbon
Nitrogen
Oxygen

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Quantity Elements

(7)

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Essential Trace Elements

(9)

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Elements that are Pervasive but no identified biological Funtion in humans

(3)

B (boron)
Si (silicon)
F (fluorine)

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Periodic Table

There are elements that are in low quantities that are of high importance
organic elements: dark green
Quantity elements: macro minerals - which are bulk elements

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Magnesium

(and Associated Diseases)

RED: more of an acute deficit than Ca2+
hypersensitive and struggling cows: if you do not tend to them quickly you may lose them (even in 30min)
they will flail their head!– hyperesthetic –> need to work from the back as that is the safest approach
Hyperesthesia (or hyperaesthesia) is a condition that involves an abnormal increase in sensitivity to stimuli of the sense.
There is very little homeostatic regulation in ruminants - there is avery tight balance
If we increase milk yields, we are going to highten the demands and therefore increase the chance of hypoMg
OR, there is a decreased intake (stopped eating or the absorption coefficient goes down)
Absorption coefficient depends on how much the positive or negative charge in the rumen is going to be
Ration will have an effect on what the absorption coefficient is going to be

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Magnesium Deficiency: Clinical Signs

vary in the range from acute to sub-clinical
bit edgy, will startle at loud noises and clapping
may pedal with their feet
May get sudden death as a result of poor absorption of Mg in the ration

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Clinical Signs of Sub Acute Magnesium Deficiency

bit more vocal/moving a bit more
depends on it stocksman can notice these subtle signs

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Clinical Signs of Chronic Mg Deficiency

Chronic form of hypoMg is very vague and really specific
basically goes for any disease in cows (clinical conditions) –> depressed milk yield
hypoMg is associated with increased HR –> may be a good differential for hypocalcemia vs. HypoMag

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Cause of Mg Deficiency

Fresh grass tends to have low levels of Mg
may be raining or snowing out so they are inclined to eat less - more likely to get hypoMg
may be eating it and there is enough in the ration, but the absorption coefficient in the rumen is reduced ( due to K+, N being converted into ammonia which is another postively charged ion, passage rate)If we have lush grass with low levels of fiber, that passage rate will go up and the absorption of Mg will go down
Tend not to take a sample for Mg as there is no time to sample with the condition being so severe, but may want to take for reference (would be lower that .5 mmol/l in these cases)

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Treatment of Mg Deficiency

give slowly and i/v
BE IN SAFE ZONE
these animals are thrashing and throwing - be safe!
Can give teh Magnesium Sulfate but it can be pretty caustic to the skin so intravenous Ca borogluconate may be a better choice
Don’t use vein of the udder if it is too dirty, but the udder/mammary vein may be the best if clean since it is in a safe zone from kicking

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Prevenetion of Mg Deficiency

MgO is the most neutral form and tends to be fed in concentrates
If you are feeding concentrates to the milking cow, it will contain Ca as well as Mg
can give Mg bolus orally to cows that we think are prone to hypoMg (especially beef suckler cows with a calf at foot in the pasture are not getting concentrates–> will benefit bolus)
Avoid K+ rich fertilizer: fertilizer will give plants the high levels of K+ in the feed that will decrease the Mg uptake in the rumen
Mg cake is a very good way to be popular with cows

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Calcium and associated diseases

(4)

think hypocalcemic as blue cows, they are cool by touch often - not moving as much and therefore do not generate as much heat for their body to stay warm
these are all just jargin for the same thing
Overall HYPOCALCEMIA
all the same thing, milk fever often used term
*

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Calcium Homeostasis

Calcium is quite tightly regulated in mammalians ( if you are a cow, should be 2.3 to 3.2 mmol/l)
BUT, if you are a dry cow you don’t need much calcium
not much goes in, not much goes out —> absorption coefficients are rather low
Once they calve, colostrum will drain a lot of Ca out of the system and if the cow is not used to it or prepared for it, may enter negative calcium situation and hypocalcemia (due to this imbalance in the absorption of the calcium and need by colostrum)
These are the 4 different ways to manipulate Calcium supply
reabsoprtion in the kidney -excreted and being reabsorbed
bone is the biggest store of Ca in the cows, but not easy to get access to! Very slow for cows to use this reserve - even slower the older you are –>skeletal formation is rather static and inactive (takes about 2 weeks to recruit osteoclasts to break down bone and give access to Ca reserves)
kidney is rather quick to alter reabsorption of Ca and GIT is rather slow to be altered
PTH is main player for the kidney (excreted when there are low levels of Ca in the blood and will cause resorption from kidney)
and other thing is that it will activate Vitamin D3 in the kidney (Kidney is converting Vit 2D into D3 which is the most active component of Vit D) which will increase absorption of Calcium in the gut
Role of Calcitonin is uncertain in cows - would only really see where there is too much Calcium in the bloodstream which is uncommon finding in cows
Mg is a cofactor for many of these stages, including the activation of Vit D3 and the release of PTH
If mg is not present in bloodstream, these homeostatic processes wont be as effective and sometimes stores

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Subclinical Ca2+ deficiency

typically cows are still able to stand
calcium in the skeletal muscle is less susceptible to Ca deficit compared to smooth muscle
see effects in such places as the gut first (stasis of gut) or bloat in the rumen (smooth muscle will respond to the low levels of Calcium quicker)
These cows look a bit edgy (cracked out looking)
may even look like they have neurological form of ketosis or hypomagnesium (would be a differential list)
this blood calcium level would indicate subclinical hypocalcemia (If there are cases of clinical hypocalcemia in cows then you must assume that are likely cases of subclinical throughout the herd)
as a consequence of the stasis in the gut, the transition will be slower and therefore the feed intake will be slower
they will not be eating and therefore are absorbing less calcium as there is less available–> end up in this loop of being sub clinical hypocalcemic and it is a precursor to enter clinical hypocalcemia

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Clinical - moderate (Ca2+ deficiency)

often: farmers will treat this for oyu and you do not see the clinical cases
dry muzzle- stop licking nose
feel cold to touch (ears)
gut stasis affects rectum –> no feces passing
levels are even lower than prior
Present: sternal recumbency and S shape neck for hypocalcemia presentation of recumbent cow, no feces/defecation, has a high BCS (3.5-4)
problems of a fat cow when calving down harder to get up (but they are in pasture), dystocia and possible nerve damage, more likely to have negative E balance and therefore eat less and therefore have hypocalcemia.
Negative E balance and Hypocalcemia tend to go hand in hand
This could have been prevented by not having the cow be this fat before calving

Clinical - Severe

(Ca2+ deficiency)

basically floating into a coma
not able to lift into sternal recumbency
reduced CO due to the lack of calcium in the blood stream
If you have a cow with hypocalcemia and farmer cant treat it- treat as emergency
hypomagnesemia is DEF an emergency - don’t even finish dinner, go there ASAP
most of the time these hypocalcemia cases are treated by the farmer, so typically these hypocalcemia cases, we don’t see!
Levels will be well less than 1.2 mmol/L to call this severe hypocalcemia.
Note: fetal membranes can get retained and stuck as well as when the cow is hypocalcemic the uterus doesnt contract either!

Treatment of Ca2+ deficiency

Just because it is a bigger cow does not mean it needs a bigger dose!
i/v: slow (let it drip slowly)
Monitor HR - don’t be negligent for their care
Use of Mg (and others) in the bottle?- good bc cofactor for preventing hypocalcemia in the first place and aid in issues that come with giving the drip of calcium (give it slowly!)- Remember Mg is a cofactor to the Vit D3 activation and helps prevent hypocalcemia in the first place
20 and 40% are the two options
subcutaneous: deposit to prevent recurrence - can give low volume treatments sub Q - we are normally going to dip the cow into a bit of hypercalcemia with treatment (or normal) and then slowly return to hypocalcemia, but since there is a sub Q deposit of calcium from the sub Q, she won’t dip back into severe hypocalcemia
May want to give sub Q continuous calcium supply - want to give to prevent reoccurence!
if you give i/v: give it slow and monitor the heartrate! lower the bottle and let it flow in a bit slower
sometimes can get a casualty, but often rare

Recovery from Ca2+ Deficiency

smooth muscles are active again and getting into normal Ca stage - may see fetal membrane be passed
Need to get her to stand to let the nerves or muscles be aleviated –> avoid compartment syndrome
belly may disappear after because it eructated (belch)
needs to drink/eat right away
may even want to drench her (20L) with some tubing (too get in intake and calcium she needs to absorb) into the esophagus and into the rumen and put more calcium in that drink as well to make sure she has some calcium to absorb in her gut as well

Cause of Calcium Deficiency

Often demand is not meant by supply!
there is a grade of absorption in the GI tract as a factor
feed intake is also a limiting factor
fat cows tend to feed less bc they are tending to mobilize the fats and are therefore they have a depression in the feed intake
we can alter the calcium levels in a dry period and therefore up the absorption prercentage in the gut
If we lower it in the dry period, we are altering the PTH response (Vit D being upregulated and therefore absorption is being upregulated)- we can cover many of our problems by lowering levels of Ca in the dry cow ration
Cows will struggle to get to their bone reserves

Ca2+ deficiency: demand not met by supply

There are about 8kg of Ca in the bone (quite a bit)
amount available is there (up triangle) but the speed of availability is down triangle
Often demand is not meant by supply!
Where as there is a quick response in the kidney but only very little gain from that

Prevention of Calcium Def.

Can try and lower Ca rations in dry cow ration - therefore increase the absorption in the gut, if the cow calves then we are going to give the cow more calcium (milking ration) and utilize a better absorption coefficient
calcium is the biggest supplement to dairy cow ration
every milking cow will have a generally high amount of Ca in their ration - need to make sure that it is more than 100 grams per cow/day
Need to put in Mg as it is a cofactor to the calcium homeostasis
remember to consider DCAB approach and making them more susceptible to the PTH regulation
May want to drench at calving, in general may want to give a drench of caclium at calving as a preventative measure
don’t give drench when hypocalcemic already because they may not be swallowing well (smooth muscle suffers from low Ca) and then you can accidentally put it straight in the lungs which will kill them (trachea would be the path of least resistance)
Always check that they are not already hypocalcemic before you give the drench - can give afterwards if we have treated them in the vein
We can give a slow release bolus in rumen as well that allows for Ca to be released and reabsorbed

Risky Cows are….

fatter cows–> slow feed intakes
older–> can’t use bone stores of Ca efficiently
Channel Island breeds are more prone: jerseys and guernsey cattle
jersey, condition score of 4, older–> typical hypocalcemic cow
If we have a limited amount of boluses available, these would be the ones to get a bolus as they are most prone and we want to prevent it

Phosphorus

Cows with hypophosphatemia are happy downers
happy downers–> respond pretty well to phosphorus injected in the blood stream (given by Foston i/v)
best way to identify “happy downers” - give Ca first and if they don’t respond, think about P being the limiting factor
will tend to be in areas where there is lots of Ca in the soil, and therefore the feed, bc they are coregulated through PTH
bc there a lot of Ca in the feed, the calcium absorption is down regulated but that means the P is as well
Need to check for any other possible reasons for it being a downer cow - a common and sad phenomena in the dairy sector! - make sure they start eating and quickly as well

DCAB

* What this all has to with and **what Na, K, Cl, and S are all about** * relatively simple equation: has to do with positive ions (Na+ and K+) and negative ions (Cl- and S^2-) * they combined will give an indication of what the charge will be in an individual animal * DM= dry matter (not interested in water in a ration) * Sulfur is a double negative charge so it will count twice, where as others will be once * There will be many other cations and anions in a ration as well, a ration is always NEUTRAL - doesn't spark on the ground- but some of these minerals arent being absorbed as easily, will affect the charge internally (make a big difference). * Ex: if Ca2+ is paired with a poorly absorbed ion and Ca2+ is abosrbed well, calcium will be taken into the blood stream where the other is excreted

DCAB: What?

* subtract the negative ions from the positive ions * We are going to feed this to our **dry cows**, we are trying to activate her **parathyroid (PTH)** hormone homeostatic processes * **why?:** BC parathyroid hormone has to do with **Vit D and Calcium** * this is all in attempt to alter the **calcium metabolism** * **_therefore, we are going to decrease the pH in the blood --\> force these cows into a metabolic acidosis_** * do by feeding more negatively charged ions than positively charged ions - because these negatively charged ions have to be neutralized and they do this with H+ (this is why we create a metabolic acidosis) * As a consequence of it, PTH receptor will have a slightly different formation and the PTH in the circulation will be more effective as a consequence of the lowered pH * **Homeostasis of Calcium will be in turn regulated more effectively** * Therefore hoping to reduce calcium homeostasis issues * **There is often this issue near calving** - need ot prepare them in the dry period with the DCAB diet (make them slightly negatively charged)

DCAB: How do we achieve this?

* Main culprit for positively charged ration is **K+** (grasses- leaves, young grass silage, etc.) * need to remove it - don't give grass silage to these cows * instead give them hay (older plant) and even maze silage - **less K+ in the ration** * also add **anions in the diet** * all these are given as biochemically neutral, but what is being ABSORBED is the chloride and suplphate (neg. charged) - others are remaining in the GIT therefore charging the cow negatively charged and in metabolic acidosis * also slightly sneaking Mg and Calcium in indirectly (also important players in homeostasis) * Mg is a cofactor in Calcium homeostasis as well so this is another way to sneak that in * Effect of DECAB diet could even be established through the cations rather than anions indirectly by affecting their availability in the rations * **Typically not very palatable -** quite caustic to the tongue or if they are being overfed them they will refuse to eat them * MgCl can be a saturated solution in the drinking water and then have an effect on the pH of the blood stream * need to feed a relatively **dry portion** for them to drink water, grass will have a ton of water and therefore is another reason to exclude grass from the ration * The more dry components you feed them, the more likely they are to drink and then benefit from this DCAB diet approach

Anionic Salts

* Need to know the negative impact of the depressed feed intake bc it is not palatable for these dry cows, we may start them off at an already negative E balance and they are refusing to eat * These cows are transitioning from dry cows into dairy cows * If there is a negative E balance prior to calving they will start to mobilize fat as energy reserves * need to manage this properly very closely * Don't want them to slip into a negative E balance and then slip into fatty liver syndrome as a consequence

Monitoring

* In normal cows urine is about a pH of **8.0 or 9.0 (alkaline)** * They have a lot of K+ normally in the grass leaves * but this is exactly what we are trying to go against in a DCAB diet * want to aim for **no variation** within the herd, need to look at distribution (all at 6.0 rather than vary) * down to 5.0-5.5 are overdoing it and getting too severe metabolic acidosis as a consequence of it * Urine pH is just a reflection of the metabolic status of the cow * Cow will try and get rid of the chloride and rid of the sulphorus (can't get rid of these alone, need to be combined with a positively charged element (adronic acid?) which is subsequently the reason for the pH to be lower * Need to check several cows every week: some going into the dry period and some going out (quick turnout of these cows) * We want to upregulate the PTH responsiveness of the cow and how we can manipulate the calcium homeostasis

Macrominerals

* They are all **interelated** * intricate web for the homeostasis of the cows that are just about to calve or around calving * intracate web for homeostasis of the cows around calving * Treatment happens in the same bottle * signs and treatments may overlap