Rumi Endocrine 3

sihirlifil's version from 2018-02-25 18:29

Milk Fever cont'd, HyperPTH

Question Answer
Prevention of milk fever (3)Feed diets low in calcium during dry period (=last 3-4 weeks before calving)
Acidify the lactating cows' diet (add anionic salts 2-3 weeks before calving)
Make sure ration has adequate Mg2+
Which 2 molecules are 'geared up' to mobilize calcium when we feed a diet low in Ca during last 3-4 weeks before calving?Vit D, PTH
How does acidifying the blood before calving affect Ca mobilization?Allows PTH to fit on receptor (works better in acid)
What's the DCAD? what's it for?Dietary Cation-Anion difference
Estimates whether the diet will be acidogenic or alkalogenic. Goal is to create diet more negatively charged (=more anionic)
(actual DCAD equation)[Na + K + (0.15 x Ca) + (0.15 x Mg)] - [Cl + (0.20 x S) + (0.30 x P)]
Effect of dietary Ca & K on milk fever
Monitoring acidification of diet: Urine pH >8 =High incidence of milk fever
Monitoring acidification of diet: Urine pH <5.5 =Excessive acidification
Monitoring acidification of diet: Urine pH 6-6.5 =Optimum for Holsteins
Monitoring acidification of diet: Urine pH 5.5-6 =Optimum for Jerseys
How does ensuring proper ration of Mg2+ help prevent milk fever?Mg2+ needed for synth & release of PTH
What's the new prevention method?Short-term Ca binder to mimic the effx of low-Ca diet in late preg. No need for DCAD! (leads to activation of natural defense mechanisms to milk fever, EU accepted use in 2008. 400g/d optimum dose?)
Concern for other mineral binding: Mg was normal in treated cows, low P at calvint (transient)
What happened??
Nutritional 2ry HyperPTH
How does nutritional 2ry hyperparathyroidism happen?Diet low in Ca a/o Vit D & high in P
PTH increases, which increases intestinal Ca absorption --> incr bone resorption --> fibrous osteodystrophy
How does renal 2ry HyperPTH happen?Chronic kidney dz: pyelonephritis
Decreased renal blood flow = decr P removal. Incr P in system = decr in Ca2+ & decr activation of Vit D, which leads to less Ca2+ --> PTH activation --> bone resorption, fibrous osteodystrophy, increased P from bone can't be excreted


Question Answer
_________% of total body P is found in the skeleton85%
P plays a role in many metabolic processes, including?Phospholipids (cell mb integrity)
Acid-bse buffer in blood
RBC metab (2,3-DPG)
Repro fxn
How does P homeostasis happen in the rumi?Rumen microbes digest phytic acid --> incr P available for absorption (via active transport in SI)
What is the stimulus to activate Vit D?Hypophosphatemia --> Inc Vit D production --> Incr P absorption from small intestine (active transport)
Saliva has high lvls of P... how does this help?Buffers
Most recovered by intestinal absorption
_________ promotes loss of P into salivaPTH
(what stimulates secretion of PTH again?)(Hypocalcemia)
3 Disease processes of HypophosphatemiaRecumbency (severe, actue)
Postparturient hemoglobinuria
Rickets (Chronic)
Severe, actue hypophostaemia: aka? when does it happen?'Downer cow'
Onset of lactation --> P depletion
Excessive PTH causes loss of P... where? trying to retain what?Lost in urine and saliva, trying to retain Ca
Downer cow:weakness is 2ry toATP depletion
CS of severe acute hypoPAlert, willing to eat, attempt to stand but can't
Can be seen as complication of milk fever due to effects of PTH
Consider in cases that don't respond to calcium therapy
Severe acute hypoP: normal range? with dz?Norm: 4-8 mg/dL in adult, 5-8.5 in juvenile
Severe acute: <1
Chronic: 2-4
Tx of severe acute hypoPTreat milk fever
Oral (safter) or IV monosodium phosphate (precipitates wit Ca, so CANT GIVE IN SAME IV LINE. Hypocalc products are not biologically active. IV works for short-term but have to address long-term oral prob)
How does post-parturient hemoglobinuria work?2,3-DPG gets depleted in RBC, & Na/K ATPase in RBC membrane runs out of ATP --> hemolysis b/c cant maintain proper gradient across RBC
Selenium/copper deficiences may exacerbate
CS of post-partum HburiaHigh-producing cattle within 6 weeks of parturition
Decreased milk production
Anemia, icterus of sclera, hemoglobinuria
Tx of post-partum HburiaSupplement P (monosodium phosphate) IV/PO/add grain or dicalcium phosphate to diet
Blood transfusion if indicated (make sure to supplement P first! fuel to fire)
Fluid therapy (flush out kidneys in short term while we fix diet issues)
Complications of hemolysisKidneys! pigment nephropathy (from hemoglobin)
Chronic moderate hypoP =Failure to grow, inappetance, unthriftiness, decr milk production (if mke it to lactation)
Rickets: how does it happen?Low P --> normal osteoid formed, but fails to mineralize
How does rickets compare to Ca deficiency?In Ca deficiency, you get osteoporosis or fibrous osteodystrophy (rickets = normal osteoid but mineralization fails)
Signs of ricketsImproper mineralization of long bones (enlargement of epiphyses, bones are easily bent or broken)
Delayed/stunted growth
How to prevent hypoPEvaluate diet
Maintain nromal Vit D levels
Supllement P, Se, and Cu if indicated
Optimal ratio of Ca:P2:1


Question Answer
_________% of total body magnesium found in skeleton70% (small amount released when Ca released)
How much Mg found intracellularly?30%
Fxns of MgCofactor for enzymes (kinases, ATP, etc)
Needed for release of PTH (can affect Ca homeostasis!)
Works at neuromusc jxn
What does Mg do at the NM jxn?Cofactor for acetlycholinesterase (AChE)
Competes with Ca2+ to inhibit ACh release into NMJ
What's the effect of LOW Mg at the NMJ?ACh accumulation in NMJ --> hyperexcitability, tetany
What's the effect of HIGH Mg at the NMJ?ACh blockade (AChE activity) --> Paresis
In the CNS, LOW Mg causes?Excitement, irritability
In the CNS, HIGH mg causes?Sedation
How is Mg homeostasis maintained?NO HORMONE SYSTEM IN PLACE to regulate! Animals must continually ingest Mg2+ & absorb it to maintain norm lvls in ECF
Where is Mg absorbed in ADULTS?Distal GIT (abomasum, intestine)
Where is Mg absorbed in CALVES?Rumen, reticulum
How does rumen pH affect Mg absorption?Increased pH = decreased absorption
Diets high in _________ & _________ decrease Mg absorptionNitrogen, K+
Which types of diets decrease Mg absorption? (high nitrogen & K+)All forage (grain decr rumen pH)
Heavily fertilized pastures (nitrogen)
Cereal grains (dont incorporate Mg well when growing)
Rapidly growing grass pastures, esp spring or fall afer rain
How does Mg excretion occurPrimarily by kidneys
Renal dz can cause hypermagnesemia... CS?Sedation/coma
Hypomagnesemia aka? in who?Grass Tetany
Happens in grazing, lactating cattle
Causes of grass tetanyRapidly growing grasses/heavy fertilizer in feed can predispose. Seasonal predilection to spring or fall
Remember, what impedes plant uptake of Mg? how does it affect the rumen?Nitrogen & potassium (from fertilizer/soil). Impairs rumen Mg absorption
Grass tetany: EARLY CSMuscle fasciculations, aggressive behavior, bellowing, nervous attitude
Grass tetany: LATE CSRecumbent, repetitive musc contractions, convulsions, seizures
If you see this, what are you thinking? what do you want to check?
Late stage grass tetany
Check the ground for evidence of paddling!
Other causes of hypoMg?"Transport tetany" 2ry to stress & low Mg diets
"Milk tetany" in calves fed milk or replacer with no access to Mg-rich feeds
"Winter tetany" when Mg-deficient forage during cold months
Dx of hypoMgBlood measurement can be tricky Most Mg is intracellular, blood Mg may go up simply with musc dmg (confounds results)
CSF more reliable
Postmortem: Vitreous humor
Tx of hypoMg: how quick? what to be careful of?EMERGENCY!
Animals can be aggressive so be careful!
Tx of hypoMg: what do you use?IV calcium & Mg salts, follow up with oral (relapse common)
Tx of hypoMg: oral Mg composed of? how to admin?Magnesium oxide
Orogastric tube or add to feed
Tx of hypoMg: Mg enema composed of? what happens?Magnesium sulfate
Raises Mg RAPIDLY, and might cause mucosal sloughing!
Prevention of hypoMgFeed legumes, avoid rapidly growing grasses
Feed 'cool season' grasses (take up more Mg during grazing season)
Limit grazing during risky growth times
Add Mg to water or provide Mg blocks


Question Answer
Fxns of KMajor intracellular cation
Maintains resting mb potential (formation & transmission of AP)
Internal K balance =Intra vs extracellular
External K balance =Intake vs loss
Source (diet)
Elim (renal, saliva, GI, milk)
Most common cause of hypokalemiaDecreased feed intake
(Stress --> high catecholamines, incr K excr by kidney)
(Adapted to high K forages: when K intake drops suddenly, delayed renal adaptation)
WHO is at a greater risk of hypoK?Ketotic cows!
How does Ketosis treatment affect potassium lvls?Steroids have mineralocorticoid effect, which increases K excretion
IV dextrose: some spillovere causes osmotic diuresis, kidney excretes more K+
What effect does alkalosis have on K+?Low H+ ions --> trade with K+ --> drives down K+
CS of hypoK(lack of coordinated APs) Absent feces, decr rumen motility
Paretic gait, kyphosis, recumbency, S-shaped neck (like hypoCa! no resistance to correction but immediately returns to position when released)
Tachycardia, arrythmias (like hypoCa)
Dx of hypoKS-shaped neck, ileus
Clin path: Potassium <2.5 mEq/L, CK (from recumbency) & AST may be increased. Check for other electrolyte imbalances!
Tx of hypoKK supplementation (IV and PO)
IV not very effective! short activng, max admin rate = 0.5 mEq/kg/hr (causes heart attack)
Tx of hypoK: how do you do oral supplementation?Admin KCl salts via OG tube 125-250g 2x daily (hard to over-supplement)
**TREND WITH E-LYTE SUPPLEMENTATION**If feasible, oral supplementation is much more effective & safe than IV
Tx of hypoK: besides supplementation what do you have to consider?Treat ketosis if present, supportive care for recumbent (e.g. floating), access to feed & water
Prognosis poor if not standing within 24-48h of tx
Prevention of HypoKPrevent ketosis
Mineralocorticoids can cause kalliuresis (avoid steroids, Dexamethasone safer than Predef if need to use)
Monitor cattle for good appetite

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